ORIGINAL_ARTICLE
Effect of eggplant (Solanum melongena) on the metabolic syndrome: A review
Metabolic syndrome (MetS), also known as syndrome X, is a significant risk factor for cardiovascular disease incidence and mortality. Increasing age, obesity, physical inactivity, smoking, and positive family history are the risk factors associated with MetS, which increases the risk of diabetes, cardiovascular disease, hypertension, hyperlipidemia, and obesity. Chemical compounds in the treatment of metabolic complications are associated with a lack of efficacy and severe side effects. Numerous studies have described the importance of herbs and natural products to treat human diseases. Therefore, nowadays, herbs-based diets and herbal medicines are recommended for the management of various diseases. The protective effects of several herbs have been reported against MetS such as rosemary, avocado, and silymarin. Eggplant (Solanum melongena) is a rich source of phenolic and alkaloid compounds. It possesses various pharmacological effects, including, anti-oxidant, antidiabetic, antihypertensive, and antihyperlipidemic, which has been supported by numerous investigations. In this review, we evaluated the effects of eggplant on MetS and its complications comprising diabetes, high blood pressure, hyperlipidemia, and obesity. According to these studies, eggplant can control diabetes through the anti-oxidative properties and inhibition of α-amylase and α-glucosidase activity. Also, eggplant has exerted an antihypertensive effect via ACE inhibitory activity. Eggplant may have shown protective effects on hyperlipidemia and obesity via the induction of lipoprotein lipase activity and the reduction of pancreatic lipase activity.Eggplant can be useful in the treatment of MetS and its complications.
https://ijbms.mums.ac.ir/article_17743_73b548e00779bc656e273d38c7211c9d.pdf
2021-04-01
420
427
10.22038/ijbms.2021.50276.11452
Antihypertensive
Antihyperlipidemic
Aubergine
Diabetes
Eggplant
metabolic syndrome
Solanum melongena
Fatemeh
Yarmohammadi
yarmohammadif971@mums.ac.ir
1
Student Research Committee, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mahboobeh
Ghasemzadeh Rahbardar
ghasemzadeh_mahboobeh@yahoo.com
2
Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Hossein
Hosseinzadeh
hosseinzadehh@mums.ac.ir
3
Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
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ORIGINAL_ARTICLE
An updated systematic review and meta-analysis on Mycobacterium tuberculosis antibiotic resistance in Iran (2013-2020)
This updated systematic review and meta-analysis follows two aims: 1) to assess Mycobacterium tuberculosis (M. tuberculosis) antibiotic resistance in Iran from 2013 to 2020 and, 2) to assess the trend of resistance from 1999 to 2020. Several national and international databases were systematically searched through MeSH extracted keywords to identify 41 published studies addressing drug-resistant M. tuberculosis in Iran. Meta-analysis was done based on the PRISMA protocols using Comprehensive Meta-Analysis software. The average prevalence of resistance to first- and second-line anti-TB drugs, multidrug-resistant TB (MDR-TB) and extensively drug-resistant TB (XDR-TB) in new and previously treated tuberculosis (TB) cases in Iran during 2013–2020 were as follows: isoniazid 6.9%, rifampin 7.9%, ethambutol 5.7%, pyrazinamide 20.4%, para-aminosalicylic acid 4.6%, capreomycin 1.7%, cycloserine 1.8%, ethionamide 11.3%, ofloxacin 1.5%, kanamycin 3.8%, amikacin 2.2%, MDR-TB 6.3% and XDR-TB 0.9%. Based on the presented data, M. tuberculosis resistance to first- and second-line anti-TB drugs, as well as MDR-TB, was low during 2013–2020 in Iran. Furthermore, there was a declining trend in TB drug resistance from 1999 to 2020. Hence, to maintain the current decreasing trend and to control and eliminate TB infection in Iran, continuous monitoring of resistance patterns is recommended.
https://ijbms.mums.ac.ir/article_17753_49d865e670edd3a4a30a726343e1a55f.pdf
2021-04-01
428
436
10.22038/ijbms.2021.48628.11161
Antibiotic Iran Meta
analysis Mycobacterium tuberculosis Resistance
Farzad
Khademi
k_farzad@yahoo.com
1
Department of Microbiology, School of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran
LEAD_AUTHOR
Amirhossein
Sahebkar
amir_saheb2000@yahoo.com
2
Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
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36. Farazi A, Sofian M, Zarrinfar N, Katebi F, Hoseini SD, Keshavarz R. Drug resistance pattern and associated risk factors of tuberculosis patients in the central province of Iran. Caspian J Intern Med 2013; 4: 785-789.
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37. Babamahmoodi F, Mahdavi MR, Jalali H, Talebi B, Roshan P, Mahdavi M. Evaluation of gene mutations involved in drug resistance in Mycobacterium tuberculosis strains derived from tuberculosis patients in Mazandaran, Iran, 2013. Int J Mol Cell Med 2014; 3: 190-195.
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43. Habibnia S, Zaker S, Nasiri MJ, Doustdar F, Ghalavand Z, Ghalami M, Eslami G. Prevalence of multidrug-resistant tuberculosis: a six-year single-center retrospective study in Tehran, Iran. Arch Clin Infect Dis 2019; 14: e82828.
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47. Imani Fooladi AA, Babak F, Fazlollah MS, Nematollah JJ. Rapid detection of MDR–Mycobacterium tuberculosis using modified PCR-SSCP from clinical Specimens. Asian Pac J Trop Biomed 2014; 4: S165-170.
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48. Tasbiti AH, Yari S, Ghanei M, Shokrgozar MA, Fateh A, Bahrmand A. Low Levels of Extensively Drug-resistant Tuberculosis among Multidrug Resistant Tuberculosis Isolates and Their Relationship to Risk Factors: Surveillance in Tehran, Iran; 2006 to 2014. Osong Public Health Res Perspect 2017; 8: 116-123.
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50. Bahrami S, Bahrmand AR, Safarpour E, Masoumi M, Saifi M. Detection of ethambutol-resistant associated mutations in Mycobacterium tuberculosis isolates from Iran using multiplex allele-specific PCR. J Med Microbiol Infec Dis 2013: 1: 41-45.
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52. Varahram M, Nasiri MJ, Farnia P, Mozafari M, Velayati AA. A retrospective analysis of isoniazid-monoresistant tuberculosis: among Iranian pulmonary tuberculosis patients. Open Microbiol J 2014; 8: 1-5.
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55
56. Miotto P, Zhang Y, Cirillo DM, Yam WC. Drug resistance mechanisms and drug susceptibility testing for tuberculosis. Respirology 2018; 23: 1098-113.
56
ORIGINAL_ARTICLE
Subtyping β -lactamase-producing Escherichia coli strains isolated from patients with UTI by MLVA and PFGE methods
Objective(s): Strain subtyping is an important epidemiological tool to trace contamination, determine clonal relationships between different strains, and the cause of outbreaks. Current subtyping methods, however, yield less than optimal subtype discrimination. Pulsed-field gel electrophoresis is the gold standard method for Escherichia coli and Multiple-Locus Variable-number tandem repeat Analysis is a rapid PCR-based method. The purpose of this study was to evaluate MLVA and PFGE methods for subtyping β -lactamase-producing E. coli strains isolated from urinary tract infections.Materials and Methods: Overall, 230 E. coli isolates from patients with urinary tract infections were examined for antimicrobial susceptibility testing. 10-loci and 7-loci MLVA and PFGE methods were used for molecular typing of β -lactamase-producing E. coli isolates. Results: Out of 230 isolates, 130 (56.5%) β -lactamase-producing E. coli isolates were found in this study. The diversity indices of the VNTR loci showed an average diversity of 0.48 and 0.54 for 7-loci and 10-loci MLVA, respectively. The discriminatory power of PFGE showed a value of 0.87. The discordance between the methods was high. Conclusion: Our study showed that PFGE is more discriminatory than MVLA. MLVA is a PCR- based method and can generate unmistakable data, in contrast to PFGE. Optimization of polymorphic VNTR is essential to improve the discriminatory power of MLVA based on geographical region.
https://ijbms.mums.ac.ir/article_17756_aa81eeea70129a50b505db72ad1c2685.pdf
2021-04-01
437
443
10.22038/ijbms.2021.49790.11372
Beta
lactamase Escherichia coli Molecular typing Pulsed
field gel electrophoresis VNTR
Alireza
Dolatyar Dehkharghani
ardltyr@ymail.com
1
Department of Microbiology, Faculty of Advanced Sciences and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
AUTHOR
Setareh
Haghighat
setareh_haghighat@yahoo.com
2
Department of Microbiology, Faculty of Advanced Sciences and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
AUTHOR
Marjan
Rahnamaye-Farzami
marjan.farzami@gmail.com
3
Department of Microbiology, Research Center of Reference Health Laboratory, Ministry of Health and Medical Education, Tehran, Iran
AUTHOR
Masoumeh
Douraghi
douraghim@yahoo.com
4
Division of Microbiology, Department of Pathobiology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Mohammad
Rahbar
rahbar.reflab@gmail.com
5
Department of Microbiology, Research Center of Reference Health Laboratory, Ministry of Health and Medical Education, Tehran, Iran
LEAD_AUTHOR
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51
ORIGINAL_ARTICLE
Non-collagenous extracellular matrix protein dermatopontin may play a role as another component of transforming growth factor-β signaling pathway in colon carcinogenesis
Objective(s): Dermatopontin (DPT) is an extracellular matrix protein that plays roles in increasing the activity of transforming growth factor-β (TGF-β) and induction of cell quiescence. These roles suggest a tumor suppressor function for DPT. This study aimed to investigate changes in DPT gene expression in colorectal cancer providing a better understanding of its carcinogenesis.Materials and Methods: We used Matched Tumor/Normal Expression Array and Cancer Profiling Arrays I containing 34 and 7 cases of colorectal cancer and their matched controls, respectively, to test DPT expression. In addition, 38 newly diagnosed cases of colorectal cancer were enrolled and their fresh colonic tumoral and normal specimens were obtained. DPT mRNA expression was analyzed using real-time PCR. In cases with DPT under expression, exonic regions of the DPT gene were sequenced using the Sanger method.Results: In array samples, DPT expression was decreased in 82.9% (34/41), increased in 12.2% (5/41), and had no changes in 4.9% (2/41). DPT was decreased in 14 fresh samples (36.8%), while 12 cases (31.6%) showed overexpression and the others had no changes. DPT expression showed no significant difference among various tumor grades and stages. The frequencies of DPT overexpression were higher in tumors having lymph node involvement (47.7% vs 28%, P=0.59). In 2 cases mutations were detected that may be responsible for decreased expression of DPT.Conclusion: The similarities between changing patterns of DPT and TGF-β expression in colorectal cancer demonstrate that DPT may act as a pre-receptor component of the TGF-β signaling pathway in colon carcinogenesis.
https://ijbms.mums.ac.ir/article_17758_2e5b422946c2b7c06b9419a479da3522.pdf
2021-04-01
444
450
10.22038/ijbms.2021.46422.10720
Colorectal cancer Dermatopontin Real
Time PCR Sanger sequencing TGF
β
Ariane
Sadr-Nabavi
sadrnabavia@mums.ac.ir
1
Medical Genetic Research Center (MGRC), School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Samaneh
Bouromand-Noughabi
samaneh.boroumand@gmail.com
2
Department of Pathology, Faculty of Medicine, Mashhad, University of Medical Sciences, Mashhad, Iran
AUTHOR
Naser
Tayebi-Meybodi
tayebimeybodi@yahoo.com
3
Department of Pathology, Faculty of Medicine, Mashhad, University of Medical Sciences, Mashhad, Iran
AUTHOR
Kimia
Dadkhah
kimiadadkhah@yahoo.com
4
Division of Human Genetics, Immunology Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Nafiseh
Amini
nafisehamini@yahoo.com
5
Medical Genetic Research Center (MGRC), School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Alfons
Meindl
alfonsmeindl@yahoo.com
6
Frauenklinik der Technischen Universität München, Klinikum rechts der Isar, München, Germany
AUTHOR
Mohammad Reza
Abbaszadegan
abbaszadeganmr@mums.ac.ir
7
Medical Genetic Research Center (MGRC), School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1. Herszenyi L, Tulassay Z. Epidemiology of gastrointestinal and liver tumors. Eur Rev Med Pharmacol Sci 2010; 14:249-258.
1
2.Mousavi SM, Gouya MM, Ramazani R, Davanlou M, Hajsadeghi N, Seddighi Z. Cancer incidence and mortality in Iran. Ann Oncol 2009; 20:556-563.
2
3. Siegel RL, Miller KD, Fedewa SA, Ahnen DJ, Meester RGS, Barzi A, et al. Colorectal cancer statistics, 2017. CA Cancer J Clin 2017; 67:177-193.
3
4. Ardalan Khales S, Abbaszadegan MR, Abdollahi A, Raeisossadati R, Tousi MF, Forghanifard MM. SALL4 as a new biomarker for early colorectal cancers. J Cancer Res Clin Oncol 2015; 141:229-235.
4
5. Abbaszadegan MR, Tavasoli A, Velayati A, Sima HR, Vosooghinia H, Farzadnia M, et al. Stool-based DNA testing, a new noninvasive method for colorectal cancer screening, the first report from Iran. World J Gastroenterol 2007; 13:1528-1533.
5
6. Dekker E, Tanis PJ, Vleugels JLA, Kasi PM, Wallace MB. Colorectal cancer. Lancet 2019; 394:1467-1480.
6
7. Okamoto O, Fujiwara S. Dermatopontin, a novel player in the biology of the extracellular matrix. Connect Tissue Res 2006; 47:177-189.
7
8. Neame PJ, Choi HU, Rosenberg LC. The isolation and primary structure of a 22-kDa extracellular matrix protein from bovine skin. J Biol Chem 1989; 264:5474-5479.
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9. Lewandowska K, Choi HU, Rosenberg LC, Sasse J, Neame PJ, Culp LA. Extracellular matrix adhesion-promoting activities of a dermatan sulfate proteoglycan-associated protein (22K) from bovine fetal skin. J Cell Sci 1991; 99:657-668.
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10. Pochampally RR, Ylostalo J, Penfornis P, Matz RR, Smith JR, Prockop DJ. Histamine receptor H1 and dermatopontin: new downstream targets of the vitamin D receptor. J Bone Miner Res 2007; 22:1338-1349.
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11. Okamoto O, Fujiwara S, Abe M, Sato Y. Dermatopontin interacts with transforming growth factor beta and enhances its biological activity. Biochem J 1999; 337:537-541.
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12. Itatani Y, Kawada K, Sakai Y. Transforming Growth Factor-beta Signaling Pathway in Colorectal Cancer and Its Tumor Microenvironment. Int J Mol Sci 2019; 20-45.
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13. Tzen CY, Huang YW. Cloning of murine early quiescence-1 gene: The murine counterpart of dermatopontin gene can induce and be induced by cell quiescence. Exp Cell Res 2004; 294:30-38.
13
14. Yamatoji M, Kasamatsu A, Kouzu Y, Koike H, Sakamoto Y, Ogawara K, et al. Dermatopontin: a potential predictor for metastasis of human oral cancer. Int J Cancer 2012; 130:2903-2911.
14
15. Li X, Feng P, Ou J, Luo Z, Dai P, Wei D, et al. Dermatopontin is expressed in human liver and is downregulated in hepatocellular carcinoma. Biochemistry (Mosc) 2009; 74:979-985.
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16. Dahl E, Sadr-Nabavi A, Klopocki E, Betz B, Grube S, Kreutzfeld R, et al. Systematic identification and molecular characterization of genes differentially expressed in breast and ovarian cancer. J Pathol 2005; 205:21-28.
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17. Malik M, Catherino WH. Novel method to characterize primary cultures of leiomyoma and myometrium with the use of confirmatory biomarker gene arrays. Fertil Steril 2007; 87:1166-1172.
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18. Catherino WH, Leppert PC, Stenmark MH, Payson M, Potlog-Nahari C, Nieman LK, et al. Reduced dermatopontin expression is a molecular link between uterine leiomyomas and keloids. Genes Chromosomes Cancer 2004; 40:204-217.
18
19. Tsibris JC, Segars J, Coppola D, Mane S, Wilbanks GD, O’Brien WF, et al. Insights from gene arrays on the development and growth regulation of uterine leiomyomata. Fertil Steril 2002; 78:114-121.
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20. Lampropoulos P, Zizi-Sermpetzoglou A, Rizos S, Kostakis A, Nikiteas N, Papavassiliou AG. TGF-beta signalling in colon carcinogenesis. Cancer Lett 2012; 314:1-7.
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21.Akhurst RJ, Derynck R. TGF-beta signaling in cancer--a double-edged sword. Trends Cell Biol 2001; 11:S44-51.
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24. Fu Y, Feng MX, Yu J, Ma MZ, Liu XJ, Li J, et al. DNA methylation-mediated silencing of matricellular protein dermatopontin promotes hepatocellular carcinoma metastasis by alpha3beta1 integrin-Rho GTPase signaling. Oncotarget 2014; 5:6701-6715.
24
ORIGINAL_ARTICLE
The therapeutic effects of berberine plus sitagliptin in a rat model of fatty liver disease
Objective(s): Fatty liver disease (FLD) is a disorder related to accumulation of excess fat within the hepatocytes. In this study, the effects of Berberine, a natural compound, and Sitagliptin as a DPP-4 inhibitor, were observed in a rat model of FLD.Materials and Methods: Forty male rats were divided into five groups (n=6) including the control group (normal food and water), high-fat group (high-fat diet (HF) for 6 weeks), Berberine group (HF with oral administration of Berberine at 150 mg/kg for 6 weeks), Sitagliptin group (HF with oral administration of Sitagliptin at 10 mg/kg for 6 weeks), and Berberine/ Sitagliptin group (HF diet within combination with oral administration of Berberine 75 mg/kg and Sitagliptin 5 mg/kg for 6 weeks). Animals were examined for weight gain, serum and hepatic biochemical parameters, tissue histology, expression of glucose transporter type 4 (GLUT4) mRNA, and protein expression of Adiponectin receptor2 (AdipoR2) and extracellular signal-regulated kinase (ERK) and phoERK.Results: The results showed that ALT, AST, lipid profile, insulin, glucose, MDA, and TNF-α were significantly improved in high-fat rats treated with Berberine/ Sitagliptin compared with HF and Sitagliptin, and Berberine alone groups. SOD and adiponectin levels in Berberine/ Sitagliptin group were also significantly increased compared with the other groups. Immunoblot analysis showed that the expression of pho-ERK/ERK was significantly decreased and expression of AdipoR2 significantly increased in the Berberine/ Sitagliptin group compared with other groups.Conclusion: Co-administration of Berberine and Sitagliptin is an effective therapeutic regimen for conditions associated with hyperlipidemia.
https://ijbms.mums.ac.ir/article_17754_f7e7bc87a739546746ecc8f4603b49f4.pdf
2021-04-01
451
459
10.22038/ijbms.2021.52239.11822
Adiponectin receptor2 DDP
4 Glucose ttransporter type 4 Natural compound Non
alcoholic fatty liver disease Pho
ERK/ERK
Soraya
Mehrdoost
soraya_mehrdoost@yahoo.com
1
Department of Biology, Faculty of Basic Sciences, Science and Research Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Parichehreh
Yaghmaei
yaghmaei_p@srbiau.ac.ir
2
Department of Biology, Faculty of Basic Sciences, Science and Research Branch, Islamic Azad University, Tehran, Iran
LEAD_AUTHOR
Hanieh
Jafary
h-jafary@srbiau.ac.ir
3
Department of Biology, Faculty of Basic Sciences, Science and Research Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Azadeh
Ebrahim-Habibi
aehabibi@sina.tums.ac.ir
4
Biosensor Research Center, Endocrinology and Metabolism Molecular-Cellular Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
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21. Heydari M, Cornide-Petronio ME, Jiménez-Castro MB, Peralta C. Data on adiponectin from 2010 to 2020: therapeutic target and prognostic factor for liver diseases? Int J Mol Sci 2020;21:5242.
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22. Karim S, Adams DH, Lalor PF. Hepatic expression and cellular distribution of the glucose transporter family. World J Gastroenterol 2012;18:6771-6781.
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56
ORIGINAL_ARTICLE
Voltage-gated potassium channels are involved in oxymatrine-regulated islet function in rat islet β cells and INS-1 cells
Objective(s): Oxymatrine can regulate glucose metabolism. But the underlying mechanisms remain unclear. We investigated the relationship of oxymatrine and voltage-gated potassium (Kv) channel in rat islet β cells and INS-1 cells.Materials and Methods: Insulin secretion and Kv channel currents were tested by radioimmunoassay and patch-clamp technique, respectively. The INS-1 cell viability was detected using cell counting kit-8 experiments. Flowcytometry analysis and western blot were employed for cell apoptosis and protein levels, respectively. INS-1 cell proliferation was assessed by the 5-Ethynyl-2’- deoxyuridine method. Results: Oxymatrine potentiated insulin secretion at high glucose (p Conclusion: The results indicate that oxymatrine can stimulate insulin secretion and decrease kv channel currents in islet β cells. Besides, oxymatrine also increases cell viability, proliferation, and reduces cell apoptosis in INS-1 cells. The effects of oxymatrine are related to kv channels. This finding provides new insight into the mechanisms of oxymatrine-regulated islet function.
https://ijbms.mums.ac.ir/article_17755_742e709253b90b76eb5cae310ff59e81.pdf
2021-04-01
460
468
10.22038/ijbms.2021.52449.11850
Apoptosis Diabetes mellitus Insulin secretion Oxymatrine Potassium channel Voltage
gated
Jingying
Gao
13633513158@163.com
1
Department of Pediatrics, Shanxi Medical University, Taiyuan, China
LEAD_AUTHOR
Lixia
xia
xlxmedicine@163.com
2
Department of Pediatrics, Shanxi Medical University, Taiyuan, China
AUTHOR
Yuanyuan
Wei
weiyuanyuanerke@163.com
3
Department of Pediatrics, Shanxi Medical University, Taiyuan, China
AUTHOR
1. International Diabetes Federation. IDF Diabetes Atlas-9th Edition. https://diabetesatlas.org/en/.
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2. Ji L, Guo X, Guo L, Ren Q, Yu N, Zhang J. A multicenter evaluation of the performance and usability of a novel glucose monitoring system in Chinese adults with diabetes. J Diabetes Sci Technol 2017;11:290-295.
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3. Wang Z. Roles of K+ channels in regulating tumour cell proliferation and apoptosis. Pflugers Arch 2004;448:274-286.
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4. González C, Baez-Nieto D, Valencia I, Oyarzún I, Rojas P, Naranjo D, et al. K(+) channels: function-structural overview. Compr Physiol 2012;2:2087-2149.
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5. Leung YM. Voltage-gated K+ channel modulators as neuroprotective agents. Life Sci 2010;86:775-780.
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6. Tarasov A, Dusonchet J, Ashcroft F. Metabolic regulation of the pancreatic beta-cell ATP-sensitive K+ channel: a pas de deux. Diabetes 2004;53 Suppl 3: S113-122.
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7. Prinz P, Goebel-Stengel M, Teuffel P, Rose M, Klapp BF, Stengel A. Peripheral and central localization of the nesfatin-1 receptor using autoradiography in rats. Biochem Biophys Res Commun 2016;470:521-527.
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8. Ashcroft FM, Rorsman P. K (ATP) channels and islet hormone secretion: new insights and controversies. Nat Rev Endocrinol 2013;9:660-669.
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9. MacDonald PE, Wheeler MB. Voltage-dependent K (+) channels in pancreatic beta cells: role, regulation and potential as therapeutic targets. Diabetologia 2003;46:1046-1062.
9
10. Maejima Y, Horita S, Kobayashi D, Aoki M, O’hashi R, Imai R, et al. Nesfatin-1 inhibits voltage gated K+ channels in pancreatic beta cells. Peptides 2017;95:10-15.
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12. MacDonald PE, Ha XF, Wang J, Smukler SR, Sun AM, Gaisano HY, et al. Members of the Kv1 and Kv2 voltage-dependent K (+) channel families regulate insulin secretion. Mol Endocrinol 2001;15:1423-1435.
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13. Kim SJ, Widenmaier SB, Choi WS, Nian C, Ao Z, Warnock G, et al. Pancreatic β-cell prosurvival effects of the incretin hormones involve post-translational modification of Kv2.1 delayed rectifier channels. Cell Death Differ 2012;19:333-344.
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15. Zhou TT, Quan LL, Chen LP, Du T, Sun KX, Zhang JC, et al. SP6616 as a new Kv2.1 channel inhibitor efficiently promotes β-cell survival involving both PKC/Erk1/2 and CaM/PI3K/Akt signaling pathways. Cell Death Dis 2016;7:e2216.
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18. Zhang YY, Yi M, Huang YP. Oxymatrine ameliorates doxorubicin-induced cardiotoxicity in rats. Cell Physiol Biochem 2017;43:626-635.
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19. Xiao TT, Wang YY, Zhang Y, Bai CH, Shen XC. Similar to spironolactone, oxymatrine is protective in aldosterone-induced cardiomyocyte injury via inhibition of calpain and apoptosis-inducing factor signaling. Plos One 2014;9:e88856.
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20. Lu LG, Zeng MD, Mao YM, Li JQ, Wan MB, Li CZ, et al. Oxymatrine therapy for chronic hepatitis B: a randomized double-blind and placebo-controlled multi-center trial. World J Gastroenterol 2003;9:2480-2483.
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21. Wang YP, Zhao W, Xue R, Zhou ZX, Liu F, Han YX, et al. Oxymatrine inhibits hepatitis B infection with an advantage of overcoming drug-resistance. Antiviral Res 2011;89:227-231.
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22. Guo C, Zhang C, Li L, Wang Z, Xiao W, Yang Z. Hypoglycemic and hypolipidemic effects of oxymatrine in high-fat diet and streptozotocin-induced diabetic rats. Phytomedicine 2014;21:807-814.
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24. Wang SB, Jia JP. Oxymatrine attenuates diabetes-associated cognitive deficits in rats. Acta Pharmacol Sin 2014;35:331-338.
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25. Zhao P, Zhou R, Li HN, Yao WX, Qiao HQ, Wang SJ, et al. Oxymatrine attenuated hypoxic-ischemic brain damage in neonatal rats via improving antioxidant enzyme activities and inhibiting cell death. Neurochem Int 2015;89:17-27.
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26. Zhang X, Jiang W, Zhou AL, Zhao M, Jiang DR. Inhibitory effect of oxymatrine on hepatocyte apoptosis via TLR4/PI3K/Akt/GSK-3β signaling pathway. World J Gastroenterol 2017;23:3839-3849.
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49
ORIGINAL_ARTICLE
Effects of morphine and NeuroAid on the expression levels of GluN2A and GluN3A in the hippocampus and striatum of rats
Objective(s): NMDA glutamatergic receptors are heteromeric receptors with various subunits. GluN2A and GluN3A subunits specify the functional heterogeneity of NMDA receptors. These subunits play a key role in the induction of LTP and synaptic plasticity. Note that, the function of NMDA subunits has interaction with the mechanism of morphine. On the other hand, NeuroAid is a Chinese traditional medicine with neuroprotective and anti-apoptotic effects. In this study, we aimed to investigate the effect of morphine and NeuroAid on expression levels of GluN2A and GluN3A in the hippocampus and striatum of rats. Materials and Methods: Morphine sulfate (increasing doses) and NeuroAid (2.5 mg/kg) were injected intraperitoneally. Real-time PCR was used to assess gene expression.Results: The results showed that morphine increased the expression of GluN2A in the hippocampus and striatum, while NeuroAid increased the expression of both genes in the hippocampus and decreased the expression of GluN3A in the striatum. NeuroAid increased the expression of GluN3A in the hippocampus and GluN2A in the striatum of morphine-addicted rats. Conclusion: NeuroAid may have interaction with the effect of morphine on glutamatergic neurotransmission; however, this study is innovative and novel, thus, further studies are needed to better understand the effect of NeuroAid and morphine on hippocampal and striatal glutamatergic neurotransmission.
https://ijbms.mums.ac.ir/article_17736_8ebadef449deed33ae63dcad7e67cf54.pdf
2021-04-01
469
475
10.22038/ijbms.2021.52004.11787
Glutamate
Hippocampus
Morphine
NeuroAid
Striatum
Katayoun
Heshmatzad
heshmatzadk@yahoo.com
1
Cognitive and Neuroscience Research Center (CNRC), Amir-Almomenin Hospital, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
AUTHOR
Mohammad
Nasehi
mo58na@yahoo.com
2
Cognitive and Neuroscience Research Center (CNRC), Amir-Almomenin Hospital, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
LEAD_AUTHOR
Salar
Vaseghi
salarv67@yahoo.com
3
Cognitive and Neuroscience Research Center (CNRC), Amir-Almomenin Hospital, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
AUTHOR
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21. Quintard H, Borsotto M, Veyssiere J, Gandin C, Labbal F, Widmann C, et al. MLC901, a traditional Chinese medicine protects the brain against global ischemia. Neuropharmacology 2011; 61:622-631.
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24. Tomazi L, Mello CF, Schoffer AP, Girardi BA, Fruhauf PK, Rubin MA. A Nonrewarding NMDA Receptor Antagonist Impairs the Acquisition, Consolidation, and Expression of Morphine Conditioned Place Preference in Mice. Mol Neurobiol 2017; 54:710-721.
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25. Lilius TO, Viisanen H, Jokinen V, Niemi M, Kalso EA, Rauhala PV. Interactions of (2S,6S;2R,6R)-hydroxynorketamine, a secondary metabolite of (R,S)-ketamine, with morphine. Basic Clin Pharmacol Toxicol 2018; 122:481-488.
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47
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48
ORIGINAL_ARTICLE
Immunization against Pseudomonas aeruginosa using Alg-PLGA nano-vaccine
Objective(s): Pseudomonas aeruginosa is the bacterium that causes of pulmonary infection among chronically hospitalized patients. Alginate is a common surface antigen of P. aeruginosa with a constant structure that which makes it an appropriate target for vaccines. In this study, P. aeruginosa alginate was conjugated with to PLGA nanoparticles, and its immunogenicity was characterized as a vaccine.Materials and Methods: Alginate was isolated from a mucoid strain of P. aeruginosa and conjugated with to PLGA with˝ N-(3-Dimethylaminopropyl)-N′-ethylcarbodiimide hydrochloride ˝= ˝EDAC˝ and N-Hydroxysuccinimide (NHS). Chemical characterization of prepared nano-vaccine was performed using FTIR Spectroscopy, Zetasizer, and Atomic Force Microscopy (AFM). The immunogenicity of this nano-vaccine was evaluated through intramuscular injection into BALB/c mice. Four groups of mice were subjected to the injection of alginate–PLGA, and two weeks after the last administration step, opsonophagocytosis assay, IgG detection, challenge, and cytokine determination via ELISA were carried out.Results: Alginate-PLGA conjugation was corroborated by FTIR, Zetasizer, and AFM. The ELISA consequence showed that alginate was prospering in the instigation of the humoral immunity.The immunogenicity enhanced against the alginate-PLGA. Remarkably diminished bacterial titer in the spleen of the immunized mice posterior to challenge with PAO1 strain in comparison with the alginate alone and control groups.Conclusion: The bacterial burden in the spleen significantly decreased after the challenge (p <0.05). The opsonic activity was significantly increased in the alginate- PLGA group (p <0.05).
https://ijbms.mums.ac.ir/article_17745_710125b2fc602e7c597ab16a38961f17.pdf
2021-04-01
476
482
10.22038/ijbms.2021.52217.11813
Alginate
Cytokine
Opsonophagocytosis
PLGA
Pseudomonas aeruginosa
Saeid
Azimi
saeidazimi68@yahoo.com
1
Parseh Institute of Iran, Tehran, Iran
AUTHOR
Leila
Safari Zanjani
leila_safari_z2007@yahoo.com
2
Department of Cellular and Molecular Biology, Zanjan Branch, Payame Noor of Zanjan, Zanjan, Iran
LEAD_AUTHOR
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61. Safari Zanjani L, Shapouri R, Dezfulian M, Mahdavi M, Shafiee Ardestani M. Eotoxin A-PLGA nanoconjugate vaccine against Pseudomonas aeruginosa infection : protectivity in murin model. World J of Microbl and Biotechnol 2019; 35:1-9.
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62. Safari Zanjani L, Shapouri R, Dezfulian M, Mahdavi M, Shafiee Ardestani M. Protective potential of conjugated Peudomonas aeruginosa LPS-PLGA nanoparticles in mice as a nano vaccine. Iran J Immunol 2020; 17: 75-86.
62
ORIGINAL_ARTICLE
NLRP3-inflammasome activation is associated with epithelial-mesenchymal transition and progression of colorectal cancer
Objective(s): Since activation of NLRP3 inflammasome results in the production of interleukin-1β (IL 1β) and initiation of inflammation as the key players in development of cancer, this study investigated possible activation of NLRP3 inflammasome during the progression of colorectal cancer (CRC) and evaluated the role of NLRP3 inflammasome in epithelial-mesenchymal transition (EMT) process. Materials and Methods: Tissue samples were collected from cancerous (test) and adjacent normal tissues (control) of forty-three male CRC patients (18 grade I and 25 grade III). The gene expression and protein levels were determined by qRT PCR and Western blotting, respectively, and tissue morphological was examined by histopathology. Results: The gene and protein expression levels of transforming growth factor-β (TGF β), IL 1β, nuclear factor κB (NF κB), NLRP3, and caspase-1, as well as the enzyme activity of caspase-1, were significantly increased in CRC. mRNA and protein levels of TGF-β, mature IL 1β, NF κB, and NLRP3 were higher in patients with grade III. EMT markers N cadherin, vimentin, and MMP 9 markedly increased in CRC, and were higher in grade III than grade I, whereas expression of E-cadherin declined by the progression of CRC. NLRP3 protein level was inversely correlated with E-cadherin whereas it positively was correlated with IL 1β, active NF κB, N cadherin, vimentin, and MMP 9. Conclusion: This study for the first time showed that activation of NLRP3 inflammasome contributed to the progression of CRC and is correlated with the EMT process. Although the present study showed that EMT markers are positively correlated with tumor grade, further investigations are required to strongly link the EMT markers to the progression of CRC.
https://ijbms.mums.ac.ir/article_17735_15386d75d2eabedbb4d193a229f5f228.pdf
2021-04-01
483
492
10.22038/ijbms.2021.52355.11835
Colorectal neoplasms Epithelial
mesenchymal transition Inflammasome NLRP3 Transforming growth factor
β
Yasser
Marandi
yasser.marandi59@gmail.com
1
Department of Clinical Biochemistry, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
AUTHOR
Shahriar
Hashemzadeh
shahriar_90@yahoo.com
2
Department of General Surgery, Imam Reza Hospital, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Heidar
Tayebinia
tavilani@gmail.com
3
Department of Clinical Biochemistry, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
AUTHOR
Jamshid
Karimi
jamshidkarimi2013@gmail.com
4
Department of Clinical Biochemistry, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
AUTHOR
Alireza
Zamani
a_zamani@umsha.ac.ir
5
Department of Immunology, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
AUTHOR
Iraj
Khodadadi
khodadadi@umsha.ac.ir
6
Department of Clinical Biochemistry, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran Research Center for Nutrition Health, Hamadan University of Medical Sciences, Hamadan, Iran
LEAD_AUTHOR
1. Mattiuzzi C, Sanchis-Gomar F, Lippi G. Concise update on colorectal cancer epidemiology. Ann Transl Med 2019; 7:609-616.
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4. Binefa G, Rodriguez-Moranta F, Teule A, Medina-Hayas M. Colorectal cancer: from prevention to personalized medicine. World J Gastroenterol 2014; 20:6786-6808.
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5. Armaghany T, Wilson JD, Chu Q, Mills G. Genetic alterations in colorectal cancer. Gastrointest Cancer Res 2012; 5:19-27.
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6. Buhrmann C, Yazdi M, Popper B, Kunnumakkara AB, Aggarwal BB, Shakibaei M. Induction of the epithelial-to-mesenchymal transition of human colorectal cancer by human TNF-beta (lymphotoxin) and its reversal by resveratrol. Nutrients 2019; 11:704-727.
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7. Tang Y, Shu G, Yuan X, Jing N, Song J. FOXA2 functions as a suppressor of tumor metastasis by inhibition of epithelial-to-mesenchymal transition in human lung cancers. Cell Res 2011; 21:316-326.
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8. Zhu QC, Gao RY, Wu W, Qin HL. Epithelial-mesenchymal transition and its role in the pathogenesis of colorectal cancer. Asian Pac J Cancer Prev 2013; 14:2689-2698.
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9. Derynck R, Muthusamy BP, Saeteurn KY. Signaling pathway cooperation in TGF-beta-induced epithelial-mesenchymal transition. Curr Opin Cell Biol 2014; 31:56-66.
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12. Song C, He L, Zhang J, Ma H, Yuan X, Hu G, et al. Fluorofenidone attenuates pulmonary inflammation and fibrosis via inhibiting the activation of NALP3 inflammasome and IL-1beta/IL-1R1/MyD88/NF-kappaB pathway. J Cell Mol Med 2016; 20:2064-2077.
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13. Lorenz G, Darisipudi MN, Anders HJ. Canonical and non-canonical effects of the NLRP3 inflammasome in kidney inflammation and fibrosis. Nephrol Dial Transplant 2014; 29:41-48.
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14. Wang H, Wang Y, Du Q, Lu P, Fan H, Lu J, et al. Inflammasome-independent NLRP3 is required for epithelial-mesenchymal transition in colon cancer cells. Exp Cell Res 2016; 342:184-192.
14
15. Wang W, Wang X, Chun J, Vilaysane A, Clark S, French G, et al. Inflammasome-independent NLRP3 augments TGF-beta signaling in kidney epithelium. J Immunol 2013; 190:1239-1249.
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16. Rosen RD, Sapra A. TNM Classification. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2020.
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17. Nazari Soltan AS, Rashtchizadeh N, Argani H, Roshangar L, Ghorbani HA, Sanajou D, et al. Dunnione protects against experimental cisplatin-induced nephrotoxicity by modulating NQO1 and NAD(+) levels. Free Radic Res 2018; 52:808-817.
17
18. Coussens LM, Werb Z. Inflammation and cancer. Nature 2002; 420:860-867.
18
19. Lin C, Zhang J. Inflammasomes in Inflammation-Induced Cancer. Front Immunol 2017; 8:271-323.
19
20. Deng Q, Geng Y, Zhao L, Li R, Zhang Z, Li K, et al. NLRP3 inflammasomes in macrophages drive colorectal cancer metastasis to the liver. Cancer Lett 2019; 442:21-30.
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21. Kolb R, Liu GH, Janowski AM, Sutterwala FS, Zhang W. Inflammasomes in cancer: a double-edged sword. Protein Cell 2014; 5:12-20.
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22. Wang Y, Kong H, Zeng X, Liu W, Wang Z, Yan X, et al. Activation of NLRP3 inflammasome enhances the proliferation and migration of A549 lung cancer cells. Oncol Rep 2016; 35:2053-2064.
22
23. Saijo Y, Tanaka M, Miki M, Usui K, Suzuki T, Maemondo M, et al. Proinflammatory cytokine IL-1 beta promotes tumor growth of Lewis lung carcinoma by induction of angiogenic factors: in vivo analysis of tumor-stromal interaction. J Immunol 2002; 169:469-475.
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24. Yun JA, Kim SH, Hong HK, Yun SH, Kim HC, Chun HK, et al. Loss of E-Cadherin expression is associated with a poor prognosis in stage III colorectal cancer. Oncology 2014; 86:318-328.
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25. Yan X, Yan L, Liu S, Shan Z, Tian Y, Jin Z. N-cadherin, a novel prognostic biomarker, drives malignant progression of colorectal cancer. Mol Med Rep 2015; 12:2999-3006.
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26. Zhang X, Liu G, Kang Y, Dong Z, Qian Q, Ma X. N-cadherin expression is associated with acquisition of EMT phenotype and with enhanced invasion in erlotinib-resistant lung cancer cell lines. PLoS One 2013; 8:e57692.
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27. Yan HB, Wang XF, Zhang Q, Tang ZQ, Jiang YH, Fan HZ, et al. Reduced expression of the chromatin remodeling gene ARID1A enhances gastric cancer cell migration and invasion via downregulation of E-cadherin transcription. Carcinogenesis 2014; 35:867-876.
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29. Luo H, Hao X, Ge C, Zhao F, Zhu M, Chen T, et al. TC21 promotes cell motility and metastasis by regulating the expression of E-cadherin and N-cadherin in hepatocellular carcinoma. Int J Oncol 2010; 37:853-859.
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30. Hur K, Toiyama Y, Takahashi M, Balaguer F, Nagasaka T, Koike J, et al. MicroRNA-200c modulates epithelial-to-mesenchymal transition (EMT) in human colorectal cancer metastasis. Gut 2013; 62:1315-1326.
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31. Jeon M, Han J, Nam SJ, Lee JE, Kim S. Elevated IL-1beta expression induces invasiveness of triple negative breast cancer cells and is suppressed by zerumbone. Chem Biol Interact 2016; 258:126-133.
31
32. Matsumoto R, Tsuda M, Yoshida K, Tanino M, Kimura T, Nishihara H, et al. Aldo-keto reductase 1C1 induced by interleukin-1beta mediates the invasive potential and drug resistance of metastatic bladder cancer cells. Sci Rep 2016; 6:34625-34642.
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33. Bates RC, Mercurio AM. Tumor necrosis factor-alpha stimulates the epithelial-to-mesenchymal transition of human colonic organoids. Mol Biol Cell 2003; 14:1790-1800.
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35. Massague J. TGFbeta in cancer. Cell 2008; 134:215-230.
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36. Derynck R, Akhurst RJ, Balmain A. TGF-beta signaling in tumor suppression and cancer progression. Nat Genet 2001; 29:117-129.
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38. Bruna A, Darken RS, Rojo F, Ocana A, Penuelas S, Arias A, et al. High TGFbeta-Smad activity confers poor prognosis in glioma patients and promotes cell proliferation depending on the methylation of the PDGF-B gene. Cancer Cell 2007; 11:147-160.
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39. Prud’homme GJ. Pathobiology of transforming growth factor beta in cancer, fibrosis and immunologic disease, and therapeutic considerations. Lab Invest 2007; 87:1077-1091.
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40. Joseph JV, Conroy S, Tomar T, Eggens-Meijer E, Bhat K, Copray S, et al. TGF-beta is an inducer of ZEB1-dependent mesenchymal transdifferentiation in glioblastoma that is associated with tumor invasion. Cell Death Dis 2014; 5:e1443.
40
ORIGINAL_ARTICLE
Kaempferide improves oxidative stress and inflammation by inhibiting the TLR4/IκBα/NF-κB pathway in obese mice
Objective(s): Kaempferide (Ka), a major natural active component of Tagetes erecta L, has numerous pharmacological effects such as anti-obesity, anticancer, and anti-hypertension. However, there is no clear evidence that Ka is directly related to inflammation and oxidative stress in obese mice. We aimed to explore the effects of Ka on inflammation and oxidative stress and its mechanism.Materials and Methods: The obese mice were induced by a high-fat diet (HFD). The anti-obesity effect was tested by liver and body weight, liver and adiposity index, and white adipose tissue. Blood sample analysis was used to detect the hypolipidemic and hypoglycemic effects. The anti-oxidation effect was assessed using GSH, SOD, MDA, CAT, T-AOC, and other indicators. The anti-inflammatory effect was assessed using TNF-α, MCP-1, and Adiponectin. Western blot and Real-Time PCR were used to evaluate the related signaling pathways.Results: Obesity, glycolipid metabolism disorder, inflammation, and oxidative stress developed in HFD mice. These changes can be effectively alleviated by Ka treatment for 16 weeks. Further studies have suggested that these beneficial effects of Ka may be associated with inhibition of the TLR4/IκBα/NF-κB signaling pathways. Conclusion: Ka possesses important anti-obesity, hypoglycemic, and hypolipidemic effects. The mechanism may be causally associated with the TLR4/IκBα/NF-κB signaling pathway, which improves inflammation and oxidative stress.
https://ijbms.mums.ac.ir/article_17744_d8277b2de3faa8d72fbce6f30bf69d66.pdf
2021-04-01
493
498
10.22038/ijbms.2021.52690.11892
Anti
inflammatory Anti
oxidation Kaempferide Obesity TLR4
Heng
Tang
1355956791th@sina.com
1
Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, PR China
AUTHOR
Qingfu
Zeng
260651407@qq.com
2
Department of vascular surgery, The Second Affiliated Hospital of Nanchang University
AUTHOR
Nina
Ren
1355956791@qq.com
3
Guangdong Online Hospital Clinic, Guangdong Second Provincial People’s Hospital, Guangzhou 510317, PR China
AUTHOR
Yunjie
Wei
4
Taihe Hospital Shiyan, Hubei, PR China
AUTHOR
Quan
He
851557800@qq.com
5
Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, PR China
AUTHOR
Ming
Chen
chenmingcq77@163.com
6
Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, PR China
AUTHOR
Peng
Pu
pp841103@sina.com
7
Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, PR China
LEAD_AUTHOR
1. Keys A. Overweight, obesity, coronary heart disease and mortality. Nut Rev 1980; 38:297-307.
1
2. Jain SS, Ashokkumar M, Bird RP. Differential expression of TNF-α signaling molecules and ERK1 in distal and proximal colonic tumors associated with obesity. Tumor Biol 2011; 32:1005-1012.
2
3. Peairs AD, Rankin JW, Yong WL. Effects of acute ingestion of different fats on oxidative stress and inflammation in overweight and obese adults. Nutr J 2011; 10:122-123.
3
4. Peng Y, Rideout D, Rakita S, Lee J, Murr M. Diet-induced obesity associated with steatosis, oxidative stress, and inflammation in liver. Surg Obes Relat Dis 2012; 8:73-81.
4
5. Park H-K, Ahima RS. Endocrine Disorders Associated with Obesity. In: Ahima RS, editor. Metabolic Syndrome: A Comprehensive Textbook. Cham: Springer International Publishing; 2014. p. 1-18.
5
6. Feng R, Sun G, Zhang Y, Sun Q, Ju L, Sun C, et al. Short-term high-fat diet exacerbates insulin resistance and glycolipid metabolism disorders in young obese men with hyperlipemia by metabolomics analysis using UPLCQ-TOF MS. J Diabetes 2018; 11:148-160.
6
7. Dong W, Zhang X, Li D, Hao W, Meng F, Bo W, et al. Kaempferide protects against myocardial ischemia/reperfusion injury through activation of the PI3K/Akt/GSK-3β pathway. Mediators Inflamm 2017:5278218-5278230.
7
8. Dumon MF, Freneix-Clerc M, Carbonneau MA, Thomas MJ, Clerc M. Demonstration of the anti-lipid peroxidation effect of 3’,5,7-trihydroxy-4’-methoxy flavone rutinoside: in vitro study. Ann Biol Clin 1994; 52:265-270.
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9. Freneix-Clerc M, Dumon MF, Carbonneau MA, Thomas MJ, Clerc M. In vivo study of the antilipoperoxidant effect of 3’,5,7-trihydroxy-4’-methoxy flavone 7 rutinoside. Ann Biol Clin 1994, 52:171-177.
9
10. Kyung-Ah K, Gu W, In-Ah L, Eun-Ha J, Dong-Hyun K, Mathias C. High fat diet-induced gut microbiota exacerbates inflammation and obesity in mice via the TLR4 signaling pathway. PloS One 2012; 7:47713-74424.
10
11. Lin Y, Ren N, Li S, Chen M, Pu P. Novel anti-obesity effect of scutellarein and potential underlying mechanism of actions. Biomed Pharmacother 2019; 117:109042-109050.
11
12. Ouchi N, Murohara T, Shibata R, Yuasa D, Ohashi k. Adiponectin as a target in obesity-related inflammatory state. Endocr Metab Immune Disord Drug Targets 2015; 15:145-150.
12
13. Wolowczuk I. Obesity – an inflammatory state. Acta Vet Scand 2015; 57:1-1.
13
14. Escoubetlozach L, Benner C, Kaikkonen MU, Lozach J, Heinz S, Spann N, et al. Mechanisms establishing TLR4-responsive activation states of inflammatory response genes. PLoS Genet 2011; 7:1002401-1002415.
14
15. Stefanie Z, Ulmer AJ, Shoichi K, Katus HA, Holger H. TLR4-mediated inflammatory activation of human coronary artery endothelial cells by LPS. Cardiovasc Res 2002; 56:126-134.
15
16. Lee J, Burckart GJ. Nuclear factor kappa B: Important transcription factor and therapeutic target. J Clin Pharmacol 1998; 38:981-993.
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17. Verma IM, Stevenson JK, Schwarz EM, Antwerp DV, Miyamoto S. Rel/NF-κB/IκB family: Intimate tales of association and dissociation. Genes Dev 1995; 9:2723-2735.
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18. Wang R, Yu XY, Guo ZY, Wang YJ, Wu Y, Yuan YF. Inhibitory effects of salvianolic acid B on CCl4-induced hepatic fibrosis through regulating NF-κB/IκBα signaling. J Ethnopharmacol 2012; 144:592-598.
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19. Lentsch AB, Ward PA. The NFκB/IκB system in acute inflammation. Arch Immunol Ther Exp 2000; 48:59-63.
19
20. Kim SR, Bae YH, Bae SK, Choi KS, Yoon KH, Koo TH, et al. Visfatin enhances ICAM-1 and VCAM-1 expression through ROS-dependent NF-kappaB activation in endothelial cells. Mol Cell Res 2008; 1783:886-895.
20
21. Wang C, Ha X, Li W, Xu P, Zhang J. Correlation of TLR4 and KLF7 in inflammation induced by obesity. Inflammation 2016; 40:1-10.
21
22. Yajun WU, Jie SU, Huang P, Chen G, Chen S, Guiyuan L. Buddleoside prevents TNF-α-induced human aortic endothelial cells inflammatory injury through inhibiting TLR4/IκBα/NF-κB signaling pathway. Chin J Mod Appl Pharm 2017; 34:637-643.
22
23. Ko MK, Sindhu S, Parikh JG, Rao NA. The role of TLR4 activation in photoreceptor mitochondrial oxidative stress. Invest Ophthalmol Vis 2011; 52:5824-5835.
23
24. Wang L, Liu XH, Chen H, Chen ZY, Weng XD, Qiu T, et al. Picroside II protects rat kidney against ischemia/reperfusion-induced oxidative stress and inflammation by the TLR4/NF-κB pathway. Exp Ther Med 2015; 9:1253-1258.
24
25. Helmut S. Oxidative stress: a concept in redox biology and medicine. Redox Biol 2015; 4:180-183.
25
26. Djordjevic A, Spasic S, Jovanovic-Galovic A, Djordjevic R, Grubor-Lajsic G Oxidative stress in diabetic pregnancy: SOD, CAT and GSH-Px activity and lipid peroxidation products. J Matern Fetal Med 2004; 16:367-372.
26
27. Lamichhane A, Prasad S, Bhaskar N, Singh J, Pandey R. Malondialdehyde (MDA): an oxidative stress marker in type II Diabetes mellitus with and without complications. Curr Trends Biotechnol Chem Res 2013; 2:112-123.
27
28. Liang Q, Sheng Y, Jiang P, Ji L, Wang Z. The gender-dependent difference of liver GSH antioxidant system in mice and its influence on isoline-induced liver injury. Toxicology 2011; 280:61-69.
28
ORIGINAL_ARTICLE
Pathogenic role of the SP/ NK1R system in GBM cells through inhibiting the thioredoxin system
Objective(s): Glioblastoma multiforme (GBM), a highly aggressive Grade IV brain tumor, is a significant public health issue due to its poor prognosis and incurability. Neuropeptide substance P (SP) plays a critical role in GBM tumor growth and development via activation of neurokinin‐1receptor (NK1R). Moreover, SP is a pro-oxidant factor contributing to oxidative stress in various cell types. However, the link between SP and oxidative stress in cancer cells is not fully investigated. Here, we aimed to identify the effects of SP and NK1R antagonist, aprepitant, on the redox status of GBM cells.Materials and Methods: Resazurin assay was employed to determine the effect of aprepitant on viability of U87 glioblastoma cells. 2’,7’-dichlorodihydrofluorescein diacetate (H2DCFDA) assay was employed to measure the levels of intracellular reactive oxygen species (ROS). A quantitative real-time polymerase chain reaction was applied to measure the expression of proteins of the thioredoxin system. Commercial kits (ZellBio GmbH) were also used to measure the enzymatic activity of these proteins.Results: We found that SP increased ROS level in U87 GBM cells, and aprepitant significantly reduced this effect. Furthermore, we found that SP could also affect the thioredoxin system, a central antioxidant enzyme defense system. SP reduced both expression and enzymatic activity of the thioredoxin system’s proteins, Trx and thioredoxin reductase (TrxR) and these effects were significantly reduced by aprepitant. Conclusion: Our results indicated that SP activation of NK1R represented a link between oxidative stress and GBM and highlighted the need for further validations in future studies.
https://ijbms.mums.ac.ir/article_17739_68191cfb154f53cef0ea4e1bf37025d2.pdf
2021-04-01
499
505
10.22038/ijbms.2021.52902.11945
Glioblastoma multiforme
Neurokinin 1 receptor
Oxidative stress
Substance P
Thioredoxin
Fatemeh
Ghahremani
fatemeghahremani17222@gmail.com
1
Department of Biology, Faculty of Science, Hakim Sabzevari University, Sabzevar, Iran
AUTHOR
Reihaneh
Sabbaghzade
r.sabbaghzadeh@hsu.ac.ir
2
Department of Biology, Faculty of Science, Hakim Sabzevari University, Sabzevar, Iran
AUTHOR
Safieh
Ebrahimi
ebrahimis961@mums.ac.ir
3
Department of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Hosein
Javid
javidh@varastegan.ac.ir
4
Medical Laboratory Sciences Department, Varastegan Institute for Medical Sciences, Mashhad, Iran
AUTHOR
Javad
Ghahremani
bayegani@gmail.com
5
Department of Medicine, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Seyed Isaac
Hashemy
hashemyi@mums.ac.ir
6
Department of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1. Hanif F, Muzaffar K, Perveen K, Malhi SM, Simjee Sh U. glioblastoma multiforme: A review of its epidemiology and pathogenesis through clinical presentation and treatment. Asian Pac J Cancer Prev 2017; 18:3-9.
1
2. Ohka F, Natsume A, Wakabayashi T. Current trends in targeted therapies for glioblastoma multiforme. Neurol Res Int 2012; 2012:878425.
2
3. Munoz M, Covenas R. Involvement of substance P and the NK-1 receptor in cancer progression. Peptides 2013; 48:1-9.
3
4. Ebrahimi S, Javid H, Alaei A, Hashemy SI. New insight into the role of substance P/neurokinin-1 receptor system in breast cancer progression and its crosstalk with microRNAs. Clin Genet 2020; 93:322-330.
4
5. Harrison S, Geppetti P. Substance p. Int J Biochem Cell Biol 2001; 33:555-576.
5
6. Garcia-Recio S, Gascon P. Biological and pharmacological aspects of the NK1-Receptor. Biomed Res Int 2015; 2015:495704.
6
7. Suvas S. Role of substance P neuropeptide in inflammation, wound healing, and tissue homeostasis. J Immunol 2017; 199:1543-1552.
7
8. Javid H, Mohammadi F, Zahiri E, Hashemy SI. The emerging role of substance P/neurokinin-1 receptor signaling pathways in growth and development of tumor cells. J Physiol Biochem 2019; 75:415-421.
8
9. Javid H, Asadi J, Zahedi Avval F, Afshari AR, Hashemy SI. The role of substance P/neurokinin 1 receptor in the pathogenesis of esophageal squamous cell carcinoma through constitutively active PI3K/Akt/NF-kappaB signal transduction pathways. Mol Biol Rep 2020; 47:2253-2263.
9
10. Mohammadi F, Javid H, Afshari AR, Mashkani B, Hashemy SI. Substance P accelerates the progression of human esophageal squamous cell carcinoma via MMP-2, MMP-9, VEGF-A, and VEGFR1 over-expression. Mol Biol Rep 2020; 47:4263-4272.
10
11. Davoodian M, Boroumand N, Mehrabi Bahar M, Jafarian AH, Asadi M, Hashemy SI. Evaluation of serum level of substance P and tissue distribution of NK-1 receptor in breast cancer. Mol Biol Rep 2019; 46:1285-1293.
11
12. Gharaee N, Pourali L, Jafarian AH, Hashemy SI. Evaluation of serum level of substance P and tissue distribution of NK-1 receptor in endometrial cancer. Mol Biol Rep 2018;45:2257-2262.
12
13. Lorestani S, Ghahremanloo A, Jangjoo A, Abedi M, Hashemy SI. Evaluation of serum level of substance P and tissue distribution of NK-1 receptor in colorectal cancer. Mol Biol Rep 2020;47:3469-3474.
13
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59
ORIGINAL_ARTICLE
Identification of the effects of acid-resistant Lactobacillus caseimetallopeptidase gene under colon-specific promoter on the colorectal and breast cancer cell lines
Objective(s): Anti-tumor effects of Lactobacilli as normal flora have been described. In a previous study, we identified a protein isolated from the bacterium Lactobacillus casei ATCC 39392 in acidic pH conditions named metallopeptidase. Therefore, we decided to evaluate the effect of the recombinant plasmid coding metallopeptidase protein on the inhibition, proliferation, or apoptosis of the colorectal and breast cancer cell lines. Materials and Methods: Identified metallopeptidase gene of L. casei under the specific colon cancer promoter was transferred to the Human SW480 and MDA-MB231 cells. Cell viability was evaluated in these two cancer cell lines via MTT assay, apoptotic changes, and expression level of p53 and MAP2K1 genes in comparison with healthy blood cells as a control group. Results: Viability of SW480 and MDA-MB231 cells was identified at 25% and 7%, respectively. An increase in apoptotic cell death in the SW480 cell line was observed as revealed by Tunnel staining. The expression assay of TP53 and MAP2K1 genes showed that MPL protein altered gene expression in a cell type-specific manner. Tunnel analyses showed that the pronounced cytotoxic effect of pEGFP-C2/MPL plasmid on SW480 cells was mediated through apoptosis. Conclusion: These results suggest that endogenous recombinant MPL under colon specific promoter inhibits the proliferation of SW480 colorectal cancer cells by increase in MAP2K1 and P53 activation. L. casei metallopeptidase under the same circumstances could not affect the growth rate and viability of MDA-MB231 breast cancer cells in vitro.
https://ijbms.mums.ac.ir/article_17738_258ec3e422e10e3654c6ee7d53b85887.pdf
2021-04-01
506
513
10.22038/ijbms.2021.53015.11950
Apoptosis Cytotoxicity Lactobacillus casei Recombinant plasmid TP53 and MAP2K1 genes
Expression
Narges
Dadfarma
n.dadfarma@yahoo.com
1
Department of Microbiology, Faculty of Biological Sciences, North Tehran Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Jamileh
Nowroozi
nowroozij@yahoo.com
2
Department of Microbiology, Faculty of Biological Sciences, North Tehran Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Bahram
Kazemi
kazemi@sbmu.ac.ir
3
Cellular and Molecular Biology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Mojgan
Bandehpour
bandehpour@gmail.com
4
Cellular and Molecular Biology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
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2
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25. Dadfarma N, Karimi G, Nowroozi J, Nejadi N, Kazemi B, Bandehpour M. The Proteomic Analysis of Lactobacillus casei in Response to Different pHs Using Two-Dimensional Electrophoresis and MALDI TOF Mass Spectroscopy. Iran J Microbiol 2020; 12:431-436.
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29. Sidira M, Galanis A, Ypsilantis P, Karapetsas A, Progaki Z, Simopoulos C, et al. Effect of Probiotic-Fermented Milk Administration on Gastrointestinal Survival of Lactobacillus casei ATCC 393 and Modulation of Intestinal Microbial Flora. J Mol Microbiol Biotechnol 2010; 19:224–230.
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51
ORIGINAL_ARTICLE
PANC-1 cancer stem-like cell death with silybin encapsulated in polymersomes and deregulation of stemness-related miRNAs and their potential targets
Objective(s): Cancer stem cells (CSCs) have powerful self-renewal ability and tumor recurrence. Pancreatic ductal adenocarcinoma is a malignancy with high mortality rate and ˃5% survival. Silybin has anticancer and hepatoprotective properties. We loaded silybin in PEG400-OA (SPNs) and evaluated its cytotoxic effects on PANC-1 cells and PANC-1 CSCs. Materials and Methods: Spheroids from PANC-1 cells were obtained by the hanging drop method. Anti-proliferative and apoptotic functions of SPNs were evaluated in spheroids and non-spheroids with MTT, DNA fragmentation, PI and PI/AnnexinV assays. The expression of CD markers was assessed with flow cytometry. QRT-PCR was used to evaluate the expression of some miRNAs and targets. Results: IC50 of SPNs was identified to be 50 µg/ml, 45 µg/ml, and 42µg/ml, respectively after 24 hr, 48 hr, and 72 hr in PANC-1 treated cells. PI staining and PI/AnnexinV assay showed that ~20%, ~60%, and ~80%, of cells treated with 30, 50, and 60 µg/ml of SPNs were in sub-G1 and apoptosis phase, respectively. DNA degradation was confirmed after SPNS stimulation. CD24, CD44, and CD133 expression decreased after SPNs treatment both in PANC-1 spheroid cells and PANC-1 cancer cell line. Under-expression of onco-miRs (miR-21, miR-155, and miR-221), over-expression of several apoptotic potential targets of oncomiRs (Bax, Casp-9, and P53), over-expression of tumor suppressive-miRs (let-7b, miR-34a, and miR-126), and under-expression of Bcl-2 was found in SPNs-treated cells. Conclusion: We suggest that silybin encapsulated in polymersomes (SPNs) may be useful as a complementary agent for destroying both pancreatic cancer cells and pancreatic CSCs along with chemotherapeutic agents.
https://ijbms.mums.ac.ir/article_17742_9da335ff75b8c39badf5c1d7ebf88fdc.pdf
2021-04-01
514
523
10.22038/ijbms.2021.54001.12136
Cancer Stem cell
miRNA
Pancreatic Cancer
Polymersome
Silybin
Fatemeh
Tehrani
maryamtehrani86@gmail.com
1
Department of Biology, Faculty of Sciences, Rasht Branch, Islamic Azad University, Rasht, Iran
AUTHOR
Najmeh
Ranji
najmehranji@gmail.com
2
Department of Biology, Faculty of Sciences, Rasht Branch, Islamic Azad University, Rasht, Iran
LEAD_AUTHOR
Fatemeh
Kouhkan
f.kouhkan@stemcells.tec
3
Department of Biology, Faculty of Sciences, Rasht Branch, Islamic Azad University, Rasht, Iran
AUTHOR
Simzar
Hosseinzadeh
s.hosseinzadeh@sbmu.ac.ir
4
Department of Biology, Faculty of Sciences, Rasht Branch, Islamic Azad University, Rasht, Iran
AUTHOR
1. Shao Y, Zhang L, Cui L, Lou W, Wang D, Lu W, et al. LIN28B suppresses microRNA let-7b expression to promote CD44+/LIN28B+ human pancreatic cancer stem cell proliferation and invasion. Am J Cancer Res 2015;5:2643-2659.
1
2. Yang Z, Zhang Y, Tang T, Zhu Q, Shi W, Yin X, et al. Transcriptome profiling of panc-1 spheroid cells with pancreatic cancer stem cells properties cultured by a novel 3d semi-solid system. Cell Physiol Biochem 2018;47:2109-2125.
2
3. Ning X, Du Y, Ben Q, Huang L, He X, Gong Y, et al. Bulk pancreatic cancer cells can convert into cancer stem cells(CSCs) in vitro and 2 compounds can target these CSCs. Cell Cycle. 2016;15:403-412.
3
4. Peng Y, Croce CM. The role of microRNAs in human cancer. Signal Transduct Target Ther 2016;1:15004.
4
5. Maleki Zadeh M, Motamed N, Ranji N, Majidi M, Falahi F. Silibinin-induced apoptosis and downregulation of microRNA-21 and microRNA-155 in MCF-7 human breast cancer cells. J. Breast Cancer 2016;19:45-52.
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6. Haddad Y, Vallerand D, Brault A, Haddad PS. Antioxidant and hepatoprotective effects of silibinin in a rat model of nonalcoholic steatohepatitis. Evid Based Complement Alternat Med 2011;2011:nep164.
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7. Sharma A, Houshyar R, Bhosale P, Choi J-I, Gulati R, Lall C. Chemotherapy induced liver abnormalities: an imaging perspective. Clin Mol Hepatol. 2014;20:317-326.
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37
ORIGINAL_ARTICLE
Investigating the basis for the antidepressant effects of Gleditsiae spina using an integrated metabolomic strategy
Objective(s): Gleditsiae spina (GS) is a natural antidepressant but its mechanisms of action remain unclear. In the present study, taxifolin (Tax) was selected to determine the role of flavonoids in the antidepressant effects of GS.Materials and Methods: Urine samples from C57BL/6 mice were analyzed based on ultra performance liquid chromatography-quadrupole time of flight mass spectrometry (UPLC-Q/TOF-MS). Then, we investigated the therapeutic effects of GS and Tax in depression models in vivo. An integrated metabolomic approach was used to examine the metabolic profiles of GS/Tax groups and corticosterone model groups (Cor). Metabolic networks in response to GS/Tax treatment were established for the comparison of antidepressant activities.Results: Corticosterone exposure significantly increased serum levels of corticosterone but decreased serum levels of 5-hydroxytryptamine and sucrose consumption (p <0.01). Treatment with GS and Tax improved all measured variables compared to those of the corticosterone-exposed group (p < 0.01). The antidepressant effects of GS and Tax involved the regulation of pentose and glucuronate interconversions, arginine and proline metabolism, phenylalanine metabolism, taurine and hypotaurine metabolism, and the citrate cycle.Conclusion: These findings indicate that flavonoids form the pharmacodynamic basis of the antidepressant effects of GS. Moreover, our findings highlight that integrated metabolomics provides a powerful tool to study the mechanisms and material basis of Chinese herbs.
https://ijbms.mums.ac.ir/article_17737_f7da195fc293cde5dabec8ad158dfdd4.pdf
2021-04-01
524
530
10.22038/ijbms.2021.51975.11781
Biomarker
Depression
Flavonoids
Metabolomics
Metabolic profiling
Tong
Liu
liutong00021@163.com
1
School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, China
AUTHOR
Ning
Zhou
zhoun0813@163.com
2
School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, China
AUTHOR
Yangang
Cao
yxycyg@hactcm.edu.cn
3
School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, China
AUTHOR
Ruihao
Xu
582680048@qq.com
4
School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, China
AUTHOR
Zhen
Liu
1115171023@qq.com
5
School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, China
AUTHOR
Xiaoke
Zheng
zhengxk.2006@163.com
6
School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, China
LEAD_AUTHOR
Weisheng
Feng
fwsh@hactcm.edu.cn
7
School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, China
AUTHOR
1. Ahern E, Kinsella S, Semkovska M. Clinical efficacy and economic evaluation of online cognitive behavioral therapy for major depressive disorder: a systematic review and meta-analysis. Expert Rev Pharmacoecon Outcomes Res 2018;18:25-41.
1
2. Kurhe Y, Mahesh R, Gupta D, Devadoss T. QCM-4, a serotonergic type 3 receptor modulator attenuates depression co-morbid with obesity in mice: An approach based on behavioral and biochemical investigations. Eur J Pharmacol 2014;5:611-618.
2
3. Clarke TK, Obsteter J, Hall LS, Hayward C, Thomson PA, Smith BH, et al. Investigating shared aetiology between type 2 diabetes and major depressive disorder in a population based cohort. Am J Med Genet B Neuropsychiatr Genet 2017;174: 227-234.
3
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4
5. Nabavi SM, Daglia M, Braidy N, Nabavi SF. Natural products, micronutrients, and nutraceuticals for the treatment of depression: A short review. Nutr Neurosci 2017; 20:180-194.
5
6. Huang KL, Lu WC, Wang YY, Hu GC, Lu CH, Lee WY, et al. Comparison of agomelatine and selective serotonin reuptake inhibitors/serotonin-norepinephrine reuptake inhibitors in major depressive disorder: A meta-analysis of head-to-head randomized clinical trials. Aust N Z J Psychiatry 2014;48:663-671.
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7. Lee G, Bae H. Therapeutic effects of phytochemicals and medicinal herbs on depression. Biomed Res Int 2017;2017:1-11.
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8. Wang D, Wang H, Gu L. The antidepressant and cognitive improvement activities of the traditional chinese herb cistanche. Evid Based Complement Alternat Med 2017;2017:3925903.
8
9. Yi JM, Kim J, Park JS, Lee J, Lee YJ, Hong JT, et al. In vivo anti-tumor effects of the ethanol extract of Gleditsia sinensis thorns and its active constituent. Cytochalasin H Biol Pharm Bull 2015;38:909-912.
9
10. Fang LH, Wang RP, Hu SY, Teng YH, Xie WB. The effect of tou nong san on transplanted tumor growth in nude mice. Evid Based Complement Alternat Med 2015;2015:518454.
10
11. Shin TY. The extract of Gleditsiae spina inhibits mast cell-mediated allergic reactions through the inhibition of histamine release and inflammatory cytokine production. Nat Prod Res 2010;16:185-191.
11
12. Lee SJ, Park SS, Kim WJ, Moon S. Gleditsia sinensis thorn extract inhibits proliferation and TNF-ɑ-induced MMP-9 expression in vascular smooth muscle cells. Am J Chin Med 2012;40:373-386.
12
13. Li J, Jiang K, Wang LJ, Yin G, Wang J, Wang Y. HPLC-MS/MS determination of flavonoids in Gleditsiae spina for its quality assessment. Sep Sci 2018;41:1752-1763.
13
14. Yu J, Zhao L, Sun X, Sun C, Wang X. Application of choline chloride deep eutectic solvents and high-speed counter-current chromatography to the extraction and purification of flavonoids from the thorns of Gleditsia sinensis Lam. Phytochem Anal 2020.
14
15. Saito S, Yamamoto Y, Maki T, Hattori Y, Ito H, Mizuno K, et al. Taxifolin inhibits amyloid-β oligomer formation and fully restores vascular integrity and memory in cerebral amyloid angiopathy. Acta Neuropathol Commun 2017;5:26-41.
15
16. Kuang H, Tang Z, Zhang C, Wang Z, Li W, Yang C, et al. Taxifolin activates the Nrf2 anti-oxidative stress pathway in mouse skin epidermal JB6 P+ cells through epigenetic modifications. Int J Mol Sci 2017;18:1546-1559.
16
17. Park SY, Kim HY, Park HJ, Shin HK, Hong KW, Kim CD. Concurrent treatment with taxifolin and cilostazol on the lowering of β-amyloid accumulation and neurotoxicity via the suppression of P-JAK2/P-STAT3/NF-κB/BACE1 signaling pathways. PLoS One 2016;11:e0168286.
17
18. Inoue T, Saito S, Tanaka M, Yamakage H, Kusakabe T, Shimatsu A, et al. Pleiotropic neuroprotective effects of taxifolin in cerebral amyloid angiopathy. Proc Natl Acad Sci USA 2019;116:10031-10038.
18
19. Gunesch S, Soriano-Castell D, Lamer S, Schlosser A, Maher P, Decker M. Development and application of a chemical probe based on a neuroprotective flavonoid hybrid for target identification using activity-based protein profiling. ACS Chem Neurosci 2020;11:3823-3837.
19
20. Liu CC, Wu YF, Feng GM, Gao XX, Zhou YZ, Hou WJ, et al. Plasma-metabolite-biomarkers for the therapeutic response in depressed patients by the traditional Chinese medicine formula Xiaoyaosan: A (1)H NMR-based metabolomics approach. Affect Disord 2015;185:156-163.
20
21. Nyer M, Mischoulon D, Alpert JE, Holt DJ, Brill CD, Yeung A, et al. College students with depressive symptoms with and without fatigue: Differences in functioning, suicidality, anxiety, and depressive severity. Ann Clin Psychiatry 2015; 27:100-108.
21
22. Enko D, Wagner H, Kriegshäuser G, Brandmayr W, Halwachs-Baumann G, Schnedl WJ, et al. Assessment of tryptophan metabolism and signs of depression in individuals with carbohydrate malabsorption. Psychiatry Res 2018;262:595-599.
22
23. Wurtman RJ, Wurtman JJ. Brain serotonin, carbohydrate-craving, obesity and depression. Obes Res 1995;Suppl 4:477-480.
23
24. Umar S, van der Laarse A. Nitric oxide and nitric oxide synthase isoforms in the normal, hypertrophic, and failing heart. Mol Cell Biochem 2010;333:191-201.
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31. Hess S, Baker G, Gyenes G, Tsuyuki R, Newman S, Melledo LJM. Decreased serum L-arginine and L-citrulline levels in major depression. Psychopharmacology 2017;234:3241-3247.
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32. Ali-Sisto T, Tolmunen T, Viinamäki H, Mäntyselkä P, Valkonen-Korhonen M, Koivumaa-Honkanen H, et al. Global arginine bioavailability ratio is decreased in patients with major depressive disorder. J Affect Disord 2018;229:145-151.
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The results described in this paper were part of student thesis.
52
Conflicts of interest
53
There are no conflicts to declare.
54
Acknowledgements
55
This work was supported by the Central Leading Local Science and Technology Development Special Foundation ((2016)149). Henan Province High-level Personnel Special Support (ZYQR201810080). Chinese National Natural Science Foundation (81903805).
56
1. Ahern E, Kinsella S, Semkovska M. Clinical efficacy and economic evaluation of online cognitive behavioral therapy for major depressive disorder: a systematic review and meta-analysis. Expert Rev Pharmacoecon Outcomes Res 2018;18:25-41.
57
2. Kurhe Y, Mahesh R, Gupta D, Devadoss T. QCM-4, a serotonergic type 3 receptor modulator attenuates depression co-morbid with obesity in mice: an approach based on behavioral and biochemical investigations. Eur J Pharmacol 2014;5:611-618.
58
3. Clarke TK, Obsteter J, Hall LS, Hayward C, Thomson PA, Smith BH, et al. Investigating shared aetiology between type 2 diabetes and major depressive disorder in a population based cohort. Am J Med Genet B Neuropsychiatr Genet 2017;174: 227-234.
59
4. Schüle C. Neuroendocrinological mechanisms of actions of antidepressant drugs. J Neuroendocrinol 2007;19:213-226.
60
5. Nabavi SM, Daglia M, Braidy N, Nabavi SF. Natural products, micronutrients, and nutraceuticals for the treatment of depression: A short review. Nutr Neurosci 2017; 20:180-194.
61
6. Huang KL, Lu WC, Wang YY, Hu GC, Lu CH, Lee WY, et al. Comparison of agomelatine and selective serotonin reuptake inhibitors/serotonin-norepinephrine reuptake inhibitors in major depressive disorder: A meta-analysis of head-to-head randomized clinical trials. Aust N Z J Psychiatry 2014;48:663-671.
62
7. Lee G, Bae H. Therapeutic Effects of Phytochemicals and Medicinal Herbs on Depression. Biomed Res Int 2017;2017:1-11.
63
8. Wang D, Wang H, Gu L. The Antidepressant and Cognitive Improvement Activities of the Traditional Chinese Herb Cistanche. Evid Based Complement Alternat Med 2017;2017:3925903.
64
9. Yi JM, Kim J, Park JS, Lee J, Lee YJ, Hong JT, et al. In Vivo Anti-tumor Effects of the Ethanol Extract of Gleditsia sinensis Thorns and Its Active Constituent. Cytochalasin H Biol Pharm Bull 2015;38:909-912.
65
10. Fang LH, Wang RP, Hu SY, Teng YH, Xie WB. The effect of tou nong san on transplanted tumor growth in nude mice. Evid Based Complement Alternat Med 2015;2015:518454.
66
11. Shin TY. The extract of Gleditsiae Spina inhibits mast cell-mediated allergic reactions through the inhibition of histamine release and inflammatory cytokine production. Nat Prod Res 2010;16:185-191.
67
12. Lee SJ, Park SS, Kim WJ, Moon S. Gleditsia sinensis thorn extract inhibits proliferation and TNF-ɑ-induced MMP-9 expression in vascular smooth muscle cells. Am J Chin Med 2012;40:373-386.
68
13. Li J, Jiang K, Wang LJ, Yin G, Wang J, Wang Y. HPLC-MS/MS determination of flavonoids in Gleditsiae Spina for its quality assessment. Sep Sci 2018;41:1752-1763.
69
14. Yu J, Zhao L, Sun X, Sun C, Wang X. Application of choline chloride deep eutectic solvents and high-speed counter-current chromatography to the extraction and purification of flavonoids from the thorns of Gleditsia sinensis Lam. Phytochem Anal 2020;17.
70
15. Saito S, Yamamoto Y, Maki T, Hattori Y, Ito H, Mizuno K, et al. Taxifolin inhibits amyloid-β oligomer formation and fully restores vascular integrity and memory in cerebral amyloid angiopathy. Acta Neuropathol Commun 2017;5:26.
71
16. Kuang H, Tang Z, Zhang C, Wang Z, Li W, Yang C, et al. Taxifolin Activates the Nrf2 Anti-Oxidative Stress Pathway in Mouse Skin Epidermal JB6 P+ Cells through Epigenetic Modifications. Int J Mol Sci 2017;18:1546.
72
17. Park SY, Kim HY, Park HJ, Shin HK, Hong KW, Kim CD. Concurrent Treatment with Taxifolin and Cilostazol on the Lowering of β-Amyloid Accumulation and Neurotoxicity via the Suppression of P-JAK2/P-STAT3/NF-κB/BACE1 Signaling Pathways. PLoS One 2016;11:e0168286.
73
18. Inoue T, Saito S, Tanaka M, Yamakage H, Kusakabe T, Shimatsu A, et al. Pleiotropic neuroprotective effects of taxifolin in cerebral amyloid angiopathy. Proc Natl Acad Sci USA 2019;116:10031-10038.
74
19. Gunesch S, Soriano-Castell D, Lamer S, Schlosser A, Maher P, Decker M. Development and Application of a Chemical Probe Based on a Neuroprotective Flavonoid Hybrid for Target Identification Using Activity-Based Protein Profiling. ACS Chem Neurosci 2020;11:3823-3837.
75
Liu CC, Wu YF, Feng GM, Gao XX, Zhou YZ, Hou WJ, et al. Plasma-metabolite-biomarkers for the therapeutic response in depressed patients by the traditional Chinese medicine formula Xiaoyaosan: A (1)H NMR-based metabolomics approach. Affect Disord 2015;185:156-163.
76
Nyer M, Mischoulon D, Alpert JE, Holt DJ, Brill CD, Yeung A, et al. College students with depressive symptoms with and without fatigue: Differences in functioning, suicidality, anxiety, and depressive severity. Ann Clin Psychiatry 2015; 27:100-108.
77
Enko D, Wagner H, Kriegshäuser G, Brandmayr W, Halwachs-Baumann G, Schnedl WJ, et al. Assessment of tryptophan metabolism and signs of depression in individuals with carbohydrate malabsorption. Psychiatry Res 2018;262:595-599.
78
Wurtman RJ, Wurtman JJ. Brain serotonin, carbohydrate-craving, obesity and depression. Obes Res 1995;Suppl 4:477-480.
79
Umar S, van der Laarse A. Nitric oxide and nitric oxide synthase isoforms in the normal, hypertrophic, and failing heart. Mol Cell Biochem 2010;333:191-201.
80
Böger RH. The pharmacodynamics of L-arginine. Altern Ther Health Med 2014;20:48-54.
81
He HY, Henderson AC, Du YL, Ryan KS. Two-Enzyme Pathway Links l-Arginine to Nitric Oxide in N-Nitroso Biosynthesis. J Am Chem Soc 2019;141:4026-4033.
82
Chong CM, Ai N, Ke M, Tan Y, Huang Z, Li Y, et al. Roles of Nitric Oxide Synthase Isoforms in Neurogenesis. Mol Neurobiol 2018;55:2645-2652.
83
Joca SRL, Sartim AG, Roncalho AL, Diniz CFA, Wegener G. Nitric oxide signalling and antidepressant action revisited. Cell Tissue Res 2019;377:45-58.
84
Sanders KM, Ward SM. Nitric oxide and its role as a non-adrenergic, non-cholinergic inhibitory neurotransmitter in the gastrointestinal tract. Br J Pharmacol 2019;176:212-227.
85
Zhang Q, Deng Y, Zhang W, Liu Y, Zha D. Drag-reducing polymers increase exercise tolerance in an ischemic hind-limb rat model. Vascular 2016;24:241-245.
86
Hess S, Baker G, Gyenes G, Tsuyuki R, Newman S, Melledo LJM. Decreased serum L-arginine and L-citrulline levels in major depression. Psychopharmacology 2017;234:3241-3247.
87
Ali-Sisto T, Tolmunen T, Viinamäki H, Mäntyselkä P, Valkonen-Korhonen M, Koivumaa-Honkanen H, et al. Global arginine bioavailability ratio is decreased in patients with major depressive disorder. J Affect Disord 2018;229:145-151.
88
Markus W, Rima KD. Creatine and Creatinine Metabolism. Physiol Rev 2000; 80:1107-1213.
89
Ji L, Zhao X, Zhang B, Kang L, Song W, Zhao B, et al. Slc6a8-Mediated Creatine Uptake and Accumulation Reprogram Macrophage Polarization via Regulating Cytokine Responses. Immunity 2019;51:272-284.
90
Tarnopolsky MA. Caffeine and creatine use in sport. Ann Nutr Metab 2010;57 Suppl 2:1-8.
91
Cappelletti P, Tallarita E, Rabattoni V, Campomenosi P, Sacchi S, Pollegioni L. Proline oxidase controls proline, glutamate, and glutamine cellular concentrations in a U87 glioblastoma cell line. PLoS One 2018;13:e0196283.
92
Hull J, Usmari Moraes M, Brookes E, Love S, Conway ME. Distribution of the branched-chain ɑ-ketoacid dehydrogenase complex E1ɑ subunit and glutamate dehydrogenase in the human brain and their role in neuro-metabolism. Neurochem Int 2018;112:49-58.
93
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Hansen AW, Almeida FB, Bandiera S, Pulcinelli RR, Caletti G, Agnes G, et al. Correlations between subunits of GABAA and NMDA receptors after chronic alcohol treatment or withdrawal, and the effect of taurine in the hippocampus of rats. Alcohol 2020;82:63-70.
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107
ORIGINAL_ARTICLE
Novel function of Nanos2 in expression of innate immunity genes and its probable roles in maintenance of pluripotency state
Objective(s): Cell-based therapeutic approaches have witnessed significant developments during the last decade especially after approval of MSCs based treatment of graft versus host disease. Several cell-based approaches have shown immunomodulatory behavior during regeneration following the unknown cascade of events but the exact mechanisms are yet to be defined. Clinical applications of cell-based drugs are hampered all over the world because of incomplete understanding of molecular mechanisms requiring the application of mechanistic approaches to solving the mystery. Current work has given us the idea that Nanos2 enhances the cellular pluripotency characteristics while down-regulating the innate immunity genes, simultaneously.Materials and Methods: The immunomodulatory behavior of cells was studied against cells carrying the ectopic expression of Nanos2 in comparison with Stella and Oct4 individually and simultaneously using SON vector (Stella, Nanos2 and Oct4). Results: It was observed that overexpression of Nanos2 leads to down-regulation of Interferon-Stimulated Genes (ISGs)-mRNAs such as Ifitm1, lsg15, Oas2, and Oas12. Nanos2 overexpressing MEF cells have shown restrictive inflammatory effects when cells were treated with inflammatory stimuli such as LPS and Poly (I:C). Conclusion: From our recent findings in line with many others, it can be concluded that Nanos2 acts as a coin with two sides, regulating pluripotency and immunity together which enhances resistance against inflammatory stimuli. Nanos2 could be a potential candidate as a molecular drug for management of inflammation and immunomodulation but it requires a comprehensive comparative expression analysis of innate immunity genes in vitro and in vivo.
https://ijbms.mums.ac.ir/article_17740_54820b63d0a62980506712c49ab24603.pdf
2021-04-01
531
536
10.22038/ijbms.2021.53841.12104
Immunomodulatory therapy
Inflammation
Innate immunity
Regenerative medicine
Stem cell transplantation
Monireh
Bahrami
monireh.bahrami@yahoo.com
1
Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran
AUTHOR
Maryam
Moghaddam Matin
matin@um.ac.ir
2
Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran
AUTHOR
Moein
Farshchian
moeinfarshchy@yahoo.com
3
Stem Cell and Regenerative Medicine Research Group, Iranian Academic Center for Education, Culture and Research (ACECR) Razavi Khorasan, Mashhad Branch, Iran
AUTHOR
Molood
Asadi
molood.asadi93@gmail.com
4
Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran
AUTHOR
Ahmad Reza
Bahrami
ar-bahrami@um.ac.ir
5
Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran
LEAD_AUTHOR
1. Arjmand B, Goodarzi P, Mohamadi-Jahani F, Falahzadeh K, Larijani B. Personalized regenerative medicine. Acta Medica Iranica 2017:144-149.
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2. Chu D-T, Nguyen TT, Tien NLB, Tran D-K, Jeong J-H, Anh PG, et al. Recent progress of stem cell therapy in cancer treatment: Molecular Mechanisms and Potential Applications. Cells 2020; 9: 563-581.
2
3. Mirahmadi M, Rezanejadbardaji H, Irfan-Maqsood M, Mokhtari MJ, Naderi-Meshkin H. Stem cell therapy for neurodegenerative diseases: strategies for regeneration against degeneration. J Genes Cells 2017; 3:22-38
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4. Steward C, Jarisch A. Haemopoietic stem cell transplantation for genetic disorders. Arch Dis Child 2005; 90:1259-1263.
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5. Müller P, Lemcke H, David R. Stem cell therapy in heart diseases–cell types, mechanisms and improvement strategies. Cell Physiol Biochem 2018; 48:2607-2655.
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6. Chen S, Du K, Zou C. Current progress in stem cell therapy for type 1 diabetes mellitus. Stem Cell Res Ther 2020; 11:1-13.
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7. Shah K, Zhao AG, Sumer H. New approaches to treat osteoarthritis with mesenchymal stem cells. Stem Cells Int 2018; 2018: 1-9.
7
8. Coalson E, Bishop E, Liu W, Feng Y, Spezia M, Liu B, et al. Stem cell therapy for chronic skin wounds in the era of personalized medicine: From bench to bedside. Genes Dis 2019; 6:342-358.
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9. Mount NM, Ward SJ, Kefalas P, Hyllner J. Cell-based therapy technology classifications and translational challenges. Philos Trans R Soc Lond B Biol Sci 2015; 370:1-16
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10. Aurora AB, Olson EN. Immune modulation of stem cells and regeneration. Cell stem cell 2014; 15:14-25.
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11. Petrie TA, Strand NS, Tsung-Yang C, Rabinowitz JS, Moon RT. Macrophages modulate adult zebrafish tail fin regeneration. Development 2014; 141:2581-2591.
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12. Godwin JW, Rosenthal N. Scar-free wound healing and regeneration in amphibians: immunological influences on regenerative success. Differentiation 2014; 87:66-75.
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13. Godwin JW, Pinto AR, Rosenthal NA. Chasing the recipe for a pro-regenerative immune system. Semin Cell Dev Biol 2017; 61:71-79
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14. Abnave P, Ghigo E. Role of the immune system in regeneration and its dynamic interplay with adult stem cells. Semin Cell Dev Biol 2019; 87:160-168
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15. Julier Z, Park AJ, Briquez PS, Martino MM. Promoting tissue regeneration by modulating the immune system. Acta Biomater 2017; 53:13-28.
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16. Kelly SH, Shores LS, Votaw NL, Collier JH. Biomaterial strategies for generating therapeutic immune responses. Adv Drug Deliv Rev 2017; 114:3-18.
16
17. Xia H, Li X, Gao W, Fu X, Fang RH, Zhang L, et al. Tissue repair and regeneration with endogenous stem cells. Nat Rev Mater 2018; 3:174-193.
17
18. Zhou Z, Shirakawa T, Ohbo K, Sada A, Wu Q, Hasegawa K, et al. RNA binding protein Nanos2 organizes post-transcriptional buffering system to retain primitive state of mouse spermatogonial stem cells. Dev Cell 2015; 34:96-107.
18
19. Farshchian M, Matin MM, Armant O, Geerts D, Dastpak M, Nakhaei-Rad S, et al. Suppression of dsRNA response genes and innate immunity following Oct4, Stella, and Nanos2 overexpression in mouse embryonic fibroblasts. Cytokine 2018; 106:1-11.
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20. Pino CJ, Westover AJ, Johnston KA, Buffington DA, Humes HD. Regenerative medicine and immunomodulatory therapy: insights from the kidney, heart, brain, and lung. Kidney Int Rep 2018; 3:771-783.
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21. Iismaa SE, Kaidonis X, Nicks AM, Bogush N, Kikuchi K, Naqvi N, et al. Comparative regenerative mechanisms across different mammalian tissues. NPJ Regen Med 2018; 3:1-20.
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22. De Keuckelaere E, Hulpiau P, Saeys Y, Berx G, Van Roy F. Nanos genes and their role in development and beyond. Cell Mol Life Sci 2018; 75:1929-1946.
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23. Wu X, Thi VLD, Huang Y, Billerbeck E, Saha D, Hoffmann H-H, et al. Intrinsic immunity shapes viral resistance of stem cells. Cell 2018; 172:423-438
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24. Guo YL. The underdeveloped innate immunity in embryonic stem cells: The molecular basis and biological perspectives from early embryogenesis. Am J Reprod Immunol 2019; 81:e13089.
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25. Chen L-L, Yang L, Carmichael G. Molecular basis for an attenuated cytoplasmic dsRNA response in human embryonic stem cells. Cell Cycle 2010; 9:3552-3564.
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26. Wang R, Teng C, Spangler J, Wang J, Huang F, Guo Y-L. Mouse embryonic stem cells have underdeveloped antiviral mechanisms that can be exploited for the development of mRNA-mediated gene expression strategy. Stem Cells Dev 2014; 23:594-604.
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27. D’Angelo W, Chen B, Gurung C, Guo Y-L. Characterization of embryonic stem cell-differentiated fibroblasts as mesenchymal stem cells with robust expansion capacity and attenuated innate immunity. Stem Cell Res Ther 2018; 9:1-12.
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28. Cullen BR, Cherry S. Is RNA interference a physiologically relevant innate antiviral immune response in mammals? Cell Host Microbe 2013; 14:374-378.
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29. Maillard PV, Van der Veen AG, Deddouche‐Grass S, Rogers NC, Merits A, Reis e Sousa C. Inactivation of the type I interferon pathway reveals long double‐stranded RNA‐mediated RNA interference in mammalian cells. EMBO J 2016; 35:2505-2518.
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30. Guo YL. Utilization of different anti‐viral mechanisms by mammalian embryonic stem cells and differentiated cells. Immunology Immunol Cell Biol 2017; 95:17-23.
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32. Fan J-B, Miyauchi-Ishida S, Arimoto K-i, Liu D, Yan M, Liu C-W, et al. Type I IFN induces protein ISGylation to enhance cytokine expression and augments colonic inflammation. Proc Natl Acad Sci U S A 2015; 112:14313-14318.
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40
ORIGINAL_ARTICLE
Down-regulation of immune checkpoints by doxorubicin and carboplatin-containing neoadjuvant regimens in a murine breast cancer model
Objective(s): Immune checkpoint expression on tumor-infiltrating lymphocytes (TILs) has a correlation with the outcome of neoadjuvant chemotherapy (NAC) in breast cancer. However, the reciprocal effect of these regimens on the quality and quantity of immune checkpoints has hitherto not been addressed. We aimed to evaluate the impact of three NAC regimens on TILs and immune checkpoints in a murine triple-negative breast cancer model.Materials and Methods: Syngeneic model of locally-advanced breast cancer was established in immunocompetent mice using a 4T1 cell line. Tumor-bearing animals were treated with human-equivalent dosages of doxorubicin, paclitaxel, paclitaxel and carboplatin combination, and placebo. Infiltration of CD3+, CD8+, and FoxP3+ cells into the tumor was assessed by immunohistochemistry. Expression of immune checkpoints, including PD-1, CTLA-4, and TIM-3, was evaluated by real-time PCR.Results: Doxorubicin led to a significant (p <0.01) increase in the percentage of the stromal infiltrating CD3+ and CD8+ lymphocytes. Doxorubicin also suppressed significantly (p <0.05) the relative expression of PD-1 compared with the placebo. PD-1 expression was significantly (p <0.05) lower in the group treated with paclitaxel and carboplatin combination as compared with the placebo. The relative expression of TIM-3 was significantly (p <0.05) suppressed in doxorubicin-treated mice in comparison with other interventions.Conclusion: Our findings hypothesize that NAC with doxorubicin may potentiate antitumor immunity not merely by recruitment of TILs, but via down-regulation of PD-1 and TIM-3 checkpoints. Carboplatin-containing NAC may suppress PD-1 as well.
https://ijbms.mums.ac.ir/article_17741_3fcd7daa042476d8fe4f8f5c5ed30319.pdf
2021-04-01
537
544
10.22038/ijbms.2021.54383.12221
Animal model Breast neoplasms Immune checkpoints Neoadjuvant chemotherapy Tumor
infiltrating
Lymphocytes
Sanambar
Sadighi
s.sadighi@tums.ac.ir
1
Department of Medical Oncology, Cancer Research Center, Cancer Institute of Iran, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Ramezanali
Sharifian
sharifir@sina.tums.ac.ir
2
Department of Hematology and Oncology, Vali-e-Asr Hospital, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Monireh
Kazemimanesh
kazemim1362@yahoo.com
3
Department of Molecular Virology, Pasteur Institute of Iran, Tehran, Iran and Université Toulouse III Paul Sabatier, INSERM U1037, Cancer Research Centre of Toulouse (CRCT), Toulouse, France
AUTHOR
Ahad
Muhammadnejad
mohamad.najad@yahoo.com
4
Cancer Biology Research Center, Cancer Institute of Iran, Tehran University of Medical Sciences
AUTHOR
Zahra
Shohosseini
shahosseinizahra@gmail.com
5
Department of Medical Biotechnology, School of Allied Medical Sciences, Iran University of Medical Sciences, Tehran, Iran
AUTHOR
Saeid
Amanpour
amanpour-s@tums.ac.ir
6
Cancer Biology Research Center, Cancer Institute of Iran, Tehran University of Medical Sciences
AUTHOR
Samad
Muhammadnejad
s-muhammadnejad@tums.ac.ir
7
Gene Therapy Research Center, Digestive Diseases Research Institute, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
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9. Silverman GJ, Azzouz DF, Mor A. Immune checkpoint inhibitors and the union of bugs against cancer. Kidney Int. 2018;93:1030–1032.
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11. Melichar B. The biology of tumor-infiltrating Leukocytes in breast cancer. Anticancer Res 2014;1126:1115–1125.
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15. Denkert C, Von Minckwitz G, Brase JC, Sinn BV, Gade S, Kronenwett R, et al. Tumor-infiltrating lymphocytes and response to neoadjuvant chemotherapy with or without carboplatin in human epidermal growth factor receptor 2-positive and triple-negative primary breast cancers. J Clin Oncol. 2015;33:983–991.
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16. Steenbrugge J, Breyne K, Demeyere K, Wever O De, Sanders NN, Broeck W Van Den, et al. Anti-inflammatory signaling by mammary tumor cells mediates prometastatic macrophage polarization in an innovative intraductal mouse model for triple-negative breast cancer. J Exp Clin Cancer Res 2018;37:191-208.
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24. Mao Y, Qu Q, Zhang Y, Liu J, Chen X, Shen K. The value of tumor infiltrating lymphocytes (TILs) for predicting response to neoadjuvant chemotherapy in breast cancer: A systematic review and meta-analysis. PLoS One 2014;9:1–21.
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29. Hu J, Zhu S, Xia X, Zhang L, Kleinerman ES, Li S. CD8+T cell-specific induction of NKG2D receptor by doxorubicin plus interleukin-12 and its contribution to CD8+T cell accumulation in tumors. Mol Cancer 2014;13:1–13.
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30. Wang YJ, Fletcher R, Yu J, Zhang L. Immunogenic effects of chemotherapy-induced tumor cell death. Genes Dis 2018;5:194–203.
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31. Zhang Z, Yu X, Wang Z, Wu P, Huang J. Anthracyclines potentiate antitumor immunity: A new opportunity for chemoimmunotherapy. Cancer Lett 2015;369:331–335.
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32. Galluzzi L, Senovilla L, Zitvogel L, Kroemer G. The secret ally: Immunostimulation by anticancer drugs. Nat Rev Drug Discov 2012;11:215–233.
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33. Miyashita M, Sasano H, Tamaki K, Hirakawa H, Takahashi Y, Nakagawa S, et al. Prognostic significance of tumor-infiltrating CD8+ and FOXP3+ lymphocytes in residual tumors and alterations in these parameters after neoadjuvant chemotherapy in triple-negative breast cancer: A retrospective multicenter study. Breast Cancer Res 2015;17:1–13.
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34. Alizadeh D, Trad M, Hanke NT, Larmonier CB, Janikashvili N, Bernard B, et al. Doxorubicin eliminates myeloid-derived suppressor cells and enhances the efficacy of adoptive T cell transfer in breast cancer. Cancer Res 2014;74:104–118.
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53
ORIGINAL_ARTICLE
Fast antibody responses by immuno-targeting and nanotechnology strategies versus HBsAg vaccine
Objective(s): Though immunization with HBsAg has been routine since the 1980s, it has numerous limitations such as low or none humoral immune responses. Today, nanotechnology is used in vaccinology to achieve higher potency. The present study deals with the achievement of fast antibody response of humoral immune responses using immune-targeting through mannosylated nanocarriers of the vaccine.Materials and Methods: Mannose sugar and HBsAg were attached to the surface of iron oxide nanoparticles. Mannosylated iron oxide nanoparticles conjugated HBsAg (HBsAg +MLCMNP), iron oxide nanoparticles conjugated HBsAg (HBsAg +LCMNP), hepatitis B vaccine, and mere HBsAg were injected twice to BALB/c mice subcutaneously, while suitable control groups were considered. Specific total IgG antibodies were evaluated on the 7th and 14th days after the final immunization. The avidity maturation of the humoral immune response was assessed with an optimized ELISA. Graph pad prism software was used to analyze statistical data. Results: Results showed that on the seventh day of the final shooting, the mannosylated nano-vaccine caused higher antibody response induction than nano-vaccine without mannose and commercial vaccine groups. After 14 days of the second injection, a significant difference was seen versus the nano-vaccine without mannose but not the commercial vaccine group. In addition, the avidity index in mannosylated nano-vaccine showed a significant increase compared with the nano-vaccine without mannose and mere HBsAg group but not compared with the commercial vaccine.Conclusion: It seems that mannosylated nano-vaccine has more potency to achieve fast antibody responses and also higher quality of humoral immune response.
https://ijbms.mums.ac.ir/article_17757_dd491c852a6b8959dec7f51b16a34f6f.pdf
2021-04-01
545
550
10.22038/ijbms.2021.52715.11896
Avidity index
Hepatitis B
Immune response
Iron oxide nanoparticle
Mannose
Mahsa
Rezaei
mahsa.rezaei1369@yahoo.com
1
Department of Biology, Sciences and Research Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Seyed Nezamedin
Hosseini
seyyednezam@yahoo.com
2
Department of Hepatitis B Vaccine Production, Production and Research Complex, Pasteur Institute of Iran, Tehran, Iran
LEAD_AUTHOR
Ramazan Ali
Khavari-Nejad
khavarinejad@tum.ac.ir
3
Department of Biology, Sciences and Research Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Farhood
Najafi
farhoodnajafi@yahoo.com
4
Department of Resin and Additives, Institute for Color Science and Technology, Tehran, Iran
AUTHOR
Mehdi
Mahdavi
mahdavivac@gmail.com
5
Recombinant Vaccine Research Center, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
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