ORIGINAL_ARTICLE
Why whey? Camel whey protein as a new dietary approach to the management of free radicals and for the treatment of different health disorders
The balance between free radicals and antioxidants is an important factor for maintaining health and slowing disease progression. The use of antioxidants, particularly natural antioxidants, has become an important strategy for dealing with this cause of widespread diseases. Natural antioxidants have been used as therapeutic tools against many diseases because they are safe, effective, and inexpensive and are among the most commonly used adjuvants in the treatment of several diseases. Camel whey protein (CWP) is considered a strong natural antioxidant because it decreases oxidative stress, enhances immune system function, and increases glutathione levels. The structure of CWP is very similar to that of other types of whey protein from different types of milk. CWP contains many components, such as lactoferrin (LF), lactalbumin, lactoglobulins, lactoperoxidase, and lysozyme, and is rich in immunoglobulins. However, in contrast to other WPs, CWP lacks β-lactoglobulin, the main cause of milk allergies in children. The components of CWP have many beneficial effects, including stimulation of both innate and adaptive immunity and anti-inflammatory, anticancer, antibacterial, and antiviral activities. Recently, it has been shown that CWP and its unique components can facilitate the treatment of impaired diabetic wound healing. However, the molecular mechanisms underlying the protective effects of CWP in human and other animal disorders are not fully understood. Therefore, the current review presents a concise summary of the scientific evidence of the beneficial effects of CWP to support its therapeutic use in disease treatment and nutritional intervention.
https://ijbms.mums.ac.ir/article_8573_4d0348678476b2a532370cb1b0256f0c.pdf
2017-04-01
338
349
10.22038/ijbms.2017.8573
Antioxidant
Camel whey protein
Free radicals
Health problems
Inflammation
Gamal
Badr
gamal.badr@aun.edu.eg
1
Zoology Department, Faculty of Science, Assiut University, 71516 Assiut, Egypt
LEAD_AUTHOR
Nancy
Ramadan
nancykaramallah@yahoo.com
2
Zoology Department, Faculty of Science, Assiut University, 71516 Assiut, Egypt
AUTHOR
Leila
Sayed
leilahassan40@yahoo.com
3
Zoology Department, Faculty of Science, Assiut University, 71516 Assiut, Egypt
AUTHOR
Badr
M Badr
4
Department of Radiation Biology, National Centre for Radiation Research and Technology (NCRRT), Atomic Energy Authority, Egypt
AUTHOR
Hossam
M Omar
5
Zoology Department, Faculty of Science, Assiut University, 71516 Assiut, Egypt
AUTHOR
Zeliha
Selamoglu
zselamoglu@ohu.edu.tr
6
Department of Biology, Faculty of Arts and Sciences, Nigde University, Nigde, Turkey
AUTHOR
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ORIGINAL_ARTICLE
Up-regulation of miR-21 decreases chemotherapeutic effect of dendrosomal curcumin in breast cancer cells
Objective(s): Despite the good results of anticancer activities by curcumin, there are some hurdles that limit the use of curcumin as an anticancer agent. Many methods were examined to overcome this defect like the use of the dendrosomal curcumin (DNC). There is increasing evidence that miRNAs play important roles in biological processes. In this study, we focus on the roles of microRNA-21 in the anti-cancer effects of DNC in breast cancer. Materials and Methods: Also, we have used different methods such as MTT, apoptosis, cell cycle analysis, transwell migration assay and RT-PCR to find out more. Results: We observed that miR-21 decreased apoptotic cells in both cells (from 6.35% to 0.34 % and from 7.72% to 1.32% orderly) and DNC increased it. As well as, our findings indicated that cell migration capacity was increased by miR-21 over expression and was decreased by DNC. The combination of miR-21 vector transfection and DNC treatment showed lower percentage of apoptotic cells or a higher level of penetration through the membrane compared with DNC treatment alone. Furthermore, DNC induced a marked increase in the number of cells in sub G1/G1 phase and a decrease in G2/M phase of the cell cycle in both; but, we observed reverse results compared it, after transfection with miR-21 vector. Conclusion: We observed that miR-21 suppress many aspects of anti-cancer effects of DNC in breast cancer cells, it seems that co-treatment with DNC and mir-21 down-regulation may provide a clinically useful tool for drug-resistance breast cancer cells.
https://ijbms.mums.ac.ir/article_8574_9157019cdcf7d5adb21f90dde4020a98.pdf
2017-04-01
350
359
10.22038/ijbms.2017.8574
Breast Cancer
Cell cycle
Cell Proliferation
Curcumin
Dendrosomal curcumin
MicroRNA-21
Mohammad Javad
Dehghan Esmatabadi
1
Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
AUTHOR
Baharak
Farhangi
farhangi.baharak@gmail.com
2
Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
AUTHOR
Maryam
Montazeri
maryam104@yahoo.com
3
Department of Medical Biotechnology, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Hamideh
Monfared
hamideh_monfared@yahoo.com
4
Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
AUTHOR
Roohollah
Nakhaei Sistani
5
Department of Cellular Biotechnology, Faculty of Chemistry, Kashan University, Kashan, Iran
AUTHOR
Majid
Sadeghizadeh
sadeghizadeh@gmail.com
6
Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
LEAD_AUTHOR
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57
ORIGINAL_ARTICLE
A multiple-antigen detection assay for tuberculosis diagnosis based on broadly reactive polyclonal antibodies
Objective(s): Detection of circulating Mycobacterium tuberculosis (M. tuberculosis) antigens is promising in Tuberculosis (TB) diagnosis. However, not a single antigen marker has been found to be widely expressed in all TB patients. This study is aimed to prepare broadly reactive polyclonal antibodies targeting multiple antigen markers (multi-target antibodies) and evaluate their efficacies in TB diagnosis. Materials and Methods: A fusion gene consisting of 38kD, ESAT6, and CFP10 was constructed and overexpressed. The fusion polyprotein was used as an immunogen to elicit production of multi-target antibodies. Their reactivities were tested. Then, the multi-target antibodies and three corresponding antibodies elicited by each single antigen (mono-target antibodies) were evaluated with sandwich ELISA for detecting M. tuberculosis antigens. Their diagnostic efficacies for TB were also compared. Results: The polyprotein successfully elicited production of multi-target antibodies targeting 38kD, ESAT6, and CFP10 as analyzed by Western blotting. When used as coating antibodies, the multi-target antibodies were more efficient in capturing the three antigens than the corresponding mono-target antibodies. By testing clinical serum, the multi-target antibodies demonstrated significantly higher sensitivity for clinical TB diagnosis than all three mono-target antibodies. Conclusion: The multi-target antibodies allowed detecting multiple antigens simultaneously and significantly enhanced TB detection compared to routine mono-target antibodies. Our study may provide a promising strategy for TB diagnosis.
https://ijbms.mums.ac.ir/article_8575_fb0a64f8417af07c844b633f2ce0b01f.pdf
2017-04-01
360
367
10.22038/ijbms.2017.8575
Antibodies
Antigen
Diagnosis
Tuberculosis
ELISA
Zhenhua
Dai
44871232@qq.com
1
Department of Bio-diagnosis, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Beijing 100850, China
AUTHOR
Zhiqiang
Liu
biodiagnosis_liu@163.com
2
Department of Bio-diagnosis, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Beijing 100850, China
AUTHOR
Bingshui
Xiu
xbssbx@vip.sina.com
3
Department of Bio-diagnosis, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Beijing 100850, China
AUTHOR
Xiqin
Yang
yangxiqin001@163.com
4
Department of Bio-diagnosis, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Beijing 100850, China
AUTHOR
Ping
Zhao
zhaopingdiagnosis@163.com
5
Chaoyang District Centre for Disease Control and Prevention, 25 Panjiayuan Huaweili, Beijing 100029, China
AUTHOR
Xuhui
Zhang
zhanghhsnow@hotmail.com
6
Department of Bio-diagnosis, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Beijing 100850, China
AUTHOR
Cuimi
Duan
duancuimi@126.com
7
Department of Bio-diagnosis, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Beijing 100850, China
AUTHOR
Haiping
Que
qhpp2005@163.com
8
Department of Bio-diagnosis, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Beijing 100850, China
AUTHOR
Heqiu
Zhang
zhangheqiu2004@126.com
9
Department of Bio-diagnosis, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Beijing 100850, China
AUTHOR
Xiaoyan
Feng
biodiagnosis2014@163.com
10
Department of Bio-diagnosis, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Beijing 100850, China
LEAD_AUTHOR
1. Cheng Y, Xie H, Sule P, Hassounah H, Graviss EA, Kong Y, et al. Fluorogenic Probes with Substitutions at the 2 and 7 Positions of Cephalosporin are Highly BlaC-Specific for Rapid Mycobacterium Tuberculosis Detection. Angew Chem Int Ed Engl2014; 53:9360-9364.
1
2. Raja A, Ranganathan UD, Bethunaickan R. Improved diagnosis of pulmonary tuberculosis by detection of antibodies against multiple Mycobacterium tuberculosis antigens. Diagn Microbiol Infect Dis2008; 60:361-368.
2
3. Zhang X, Su Z, Hu C, Yu J, Gao Q, Wang H. Generation of Mycobacterium tuberculosis-specific recombinant antigens and evaluation of the clinical value of antibody detection for serological diagnosis of pulmonary tuberculosis. Int J Mol Med2013, 31:751-757.
3
4. Ireton GC, Greenwald R, Liang H, Esfandiari J, Lyashchenko KP, Reed SG. Identification of Mycobacterium tuberculosis antigens of high serodiagnostic value. Clin Vaccine Immunol2010, 17:1539-1547.
4
5. Zhang MM, Zhao JW, Sun ZQ, Liu J, Guo XK, Liu WD et al. Identification of RD5-encoded Mycobacterium tuberculosis proteins as B-cell antigens used for serodiagnosis of tuberculosis. Clin Dev Immunol2012; 2012:738043.
5
6. Tanimura T, Jaramillo E, Weil D, Raviglione M, Lonnroth K. Financial burden for tuberculosis patients in low- and middle-income countries: a systematic review. Eur Respir J2014; 43:1763-1775.
6
7. Brodwall K. [Diagnosis of tuberculosis in low and middle income countries]. Tidsskr Nor Laegeforen2012; 132:521.
7
8. Qi Y, Cui L, Ge Y, Shi Z, Zhao K, Guo X et al. Altered serum microRNAs as biomarkers for the early diagnosis of pulmonary tuberculosis infection. BMC Infect Dis2012; 12:384.
8
9. Adelman MW, Kurbatova E, Wang YF, Leonard MK, White N, McFarland DA et al. Cost analysis of a nucleic acid amplification test in the diagnosis of pulmonary tuberculosis at an urban hospital with a high prevalence of TB/HIV. PLoS One 2014, 9:e100649.
9
10. Belard S, Andronikou S, Pillay T, Grobusch MP, Zar HJ. New imaging approaches for improving diagnosis of childhood tuberculosis. S Afr Med J2014; 104:181-182.
10
11. Trajman A, da Silva Santos Kleiz de Oliveira EF, Bastos ML, Belo Neto E, Silva EM, da Silva Lourenco MC et al. Accuracy of polimerase chain reaction for the diagnosis of pleural tuberculosis. Respir Med2014; 108:918-923.
11
12. Baumann R, Kaempfer S, Chegou NN, Oehlmann W, Loxton AG, Kaufmann SH et al. Serologic diagnosis of tuberculosis by combining Ig classes against selected mycobacterial targets. J Infect2014; 69:581-589.
12
13. Harinath BC, Kumar S, Roy SS, Hirudkar S, Upadhye V, Shende N. A cocktail of affinity-purified antibodies reactive with diagnostically useful mycobacterial antigens ES-31, ES-43, and EST-6 for detecting the presence of Mycobacterium tuberculosis. Diagn Microbiol Infect Dis2006; 55:65-68.
13
14. Liu Z, Qie S, Li L, Xiu B, Yang X, Dai Z et al. Identification of Novel RD1 Antigens and Their combinations for diagnosis of sputum smear-/culture+ TB patients. Biomed Res Int2016; 2016:7486425.
14
15. Legesse M, Ameni G, Medhin G, Mamo G, Franken KL, Ottenhoff TH et al. IgA response to ESAT-6/CFP-10 and Rv2031 antigens varies in patients with culture-confirmed pulmonary tuberculosis, healthy Mycobacterium tuberculosis-infected and non-infected individuals in a tuberculosis endemic setting, Ethiopia. Scand J Immunol2013; 78:266-274.
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16. Majumdar A, Kamble PD, Harinath BC. Detection of circulating free and immune-complexed antigen in pulmonary tuberculosis using cocktail of antibodies to mycobacterium tuberculosis excretory secretory antigens by peroxidase enzyme immunoassay. Indian J Tuberc2010; 57:67-74.
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17. van Pinxteren LA, Ravn P, Agger EM, Pollock J, Andersen P. Diagnosis of tuberculosis based on the two specific antigens ESAT-6 and CFP10. Clin Diagn Lab Immunol2000; 7:155-160.
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18. Feng X, Yang X, Xiu B, Qie S, Dai Z, Chen K et al. IgG, IgM and IgA antibodies against the novel polyprotein in active tuberculosis. BMC Infect Dis2014; 14:336.
18
19. Feng X, Xiu B, Chen K, Yang X, Zhang H, Yue J et al. Enhanced serodiagnostic utility of novel Mycobacterium tuberculosis polyproteins. J Infect2013; 66:366-375.
19
20. Cho OH, Park KH, Park SJ, Kim SM, Park SY, Moon SM et al. Rapid diagnosis of tuberculous peritonitis by T cell-based assays on peripheral blood and peritoneal fluid mononuclear cells. J Infect2011; 62:462-471.
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21. Yan L, Xiao H, Zhang Q. Systematic review: Comparison of Xpert MTB/RIF, LAMP and SAT methods for the diagnosis of pulmonary tuberculosis. Tuberculosis (Edinb)2016; 96:75-86.
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22. Sehgal IS, Dhooria S, Aggarwal AN, Behera D, Agarwal R. Diagnostic Performance of Xpert MTB/RIF in Tuberculous Pleural Effusion: Systematic Review and Meta-analysis. J Clin Microbiol2016; 54:1133-1136.
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23. Lawn SD, Zumla AI. Tuberculosis. Lancet2011; 378:57-72.
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24. Anderson BL, Welch RJ, Litwin CM. Assessment of three commercially available serologic assays for detection of antibodies to Mycobacterium tuberculosis and identification of active tuberculosis. Clin Vaccine Immunol2008; 15:1644-1649.
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25. Kalra M, Khuller GK, Grover A, Behera D, Wanchu A, Verma I. Utility of a combination of RD1 and RD2 antigens as a diagnostic marker for tuberculosis. Diagn Microbiol Infect Dis2010; 66:153-161.
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26. Flores LL, Steingart KR, Dendukuri N, Schiller I, Minion J, Pai M et al. Systematic review and meta-analysis of antigen detection tests for the diagnosis of tuberculosis. Clin Vaccine Immunol2011; 18:1616-1627.
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27. Demkow U, Filewska M, Michalowska-Mitczuk D, Kus J, Jagodzinski J, Zielonka T et al. Heterogeneity of antibody response to myobacterial antigens in different clinical manifestations of pulmonary tuberculosis. J Physiol Pharmacol2007; 58:117-127.
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28. Deng S, Yuan T, Xia J, Huang H, Cheng X, Chen M. Clinical utility of a combination of lipoarabinomannan, 38-kDa, and 16-kDa antigens as a diagnosis tool for tuberculosis. Diagn Microbiol Infect Dis2011; 71:46-50.
28
29. Bekmurzayeva A, Sypabekova M, Kanayeva D. Tuberculosis diagnosis using immunodominant, secreted antigens of Mycobacterium tuberculosis. Tuberculosis (Edinb)2013; 93:381-388.
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30. Vordermeier HM, Whelan A, Cockle PJ, Farrant L, Palmer N, Hewinson RG. Use of synthetic peptides derived from the antigens ESAT-6 and CFP-10 for differential diagnosis of bovine tuberculosis in cattle. Clin Diagn Lab Immunol2001; 8:571-578.
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31. Parkash O, Singh BP, Pai M. Regions of differences encoded antigens as targets for immunodiagnosis of tuberculosis in humans. Scand J Immunol2009; 70:345-357.
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32. Kanekiyo M, Wei CJ, Yassine HM, McTamney PM, Boyington JC, Whittle JR et al. Self-assembling influenza nanoparticle vaccines elicit broadly neutralizing H1N1 antibodies. Nature2013; 499:102-106.
32
ORIGINAL_ARTICLE
Effects of buprenorphine in the adrenal, thyroid, and cytokine intra-operative responses in a rat model (Rattus norvegicus): a preliminary study
Objective(s): Buprenorphine is a common analgesic in experimental research, due to effectiveness and having few side-effects, including a limited influence in the immune and endocrine systems. However, how buprenorphine affects cytokine levels and the adrenal and thyroid response during general anesthesia and surgery is incompletely understood. This study aimed to assess whether buprenorphine modulated significantly those responses in rats submitted to general anesthesia, mechanical ventilation, and surgical insertion of intravascular catheters. Materials and Methods: Animals were anesthetized with isoflurane, mechanically ventilated, and surgically instrumented for carotid artery and the femoral vein catheter placement. The test group (n=16), received buprenorphine subcutaneously before surgery, whereas the control group (n=16) received normal saline. Blood sampling to determine plasma levels of adrenocorticotropic hormone (ACTH), corticosterone (CS), total thyroxine (TT4), total triiodothyronine (TT3), thyroid-stimulating hormone (TSH), TNF-α, IL6, IL10, TNF-α, IL6, and IL10 mRNA was performed at 10 min after completion of all surgical procedures and at 90, 150, 240, and 300 min thereafter, with the animals still anesthetized and with mechanical ventilation. Results: Buprenorphine-treated animals had higher levels of ACTH, CS, and TT4 at several time points (P<0.05) and TSH and TT3 at all-time points (P<0.05). They also had increased IL10, TNF-α, and IL10 mRNA levels. Conclusion: In this model, buprenorphine significantly modulated the intra-operative cytokine and endocrine response to anesthesia, mechanical ventilation, and surgical placement of intravascular catheters. The mechanism and significance of these findings remain undetermined. Researchers should be aware of these effects when considering the use of buprenorphine for analgesic purposes.
https://ijbms.mums.ac.ir/article_8576_0e87a9feb0e447bd5c92bf947bc26fd0.pdf
2017-04-01
368
379
10.22038/ijbms.2017.8576
ACTH
Buprenorphine
Corticosterone
Cytokine
Intra- surgery
Rat
Nuno
M Félix
nuno.felixgrey@gmail.com
1
Centro de Investigação Interdisciplinar em Sanidade Animal (CIISA) Faculdade de Medicina Veterinária, University of Lisbon (ULisboa), Lisboa, Portugal
LEAD_AUTHOR
Rodolfo
O Leal
2
Centre Hospitalier Vétérinaire Fregis, Arcueil, France
AUTHOR
I
Goy-Thollot
3
SIAMU, VetAgro Sup, Marcy l’Étoile, France – Université de Lyon, VetAgro Sup, EA APCSe Agressions Pulmonaires et Circulatoires dans le Sepsis, Marcy L’Etoile, France
AUTHOR
Ronald
S Walton
4
Animal Medical Center of Seattle Shoreline, Washington, USA
AUTHOR
Solange
A Gil
5
Centro de Investigação Interdisciplinar em Sanidade Animal (CIISA) Faculdade de Medicina Veterinária, University of Lisbon (ULisboa), Lisboa, Portugal
AUTHOR
Luísa
M Mateus
6
Centro de Investigação Interdisciplinar em Sanidade Animal (CIISA) Faculdade de Medicina Veterinária, University of Lisbon (ULisboa), Lisboa, Portugal
AUTHOR
Ana
S Matos
7
UNIDEMI, Departamento de Engenharia Mecânica e Industrial, Faculdade de Ciências e Tecnologia, Universidade Nova de Lisboa, Caparica, Portugal
AUTHOR
Maria
M R E Niza
8
Centro de Investigação Interdisciplinar em Sanidade Animal (CIISA) Faculdade de Medicina Veterinária, University of Lisbon (ULisboa), Lisboa, Portugal
AUTHOR
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ORIGINAL_ARTICLE
Recombinant production and affinity purification of the FraC pore forming toxin using hexa-His tag and pET expression cassette
Objective(s): A newly-introduced protein toxin from a sea anemone, namely fragaceatoxin C is a protein with molecular weight of 20 kDa and pore-forming capability against cell membranes has recently grasped great attentions for its function. In this study, its coding sequence cloned as a fusion protein with His-tag for simple production and rapid purification. Materials and Methods: After PCR amplification using NcoI and HindIII-harboring primers, the gene fragment was cloned into pET-28a(+). Escherichia coli BL21 was used for expression of constructed vector and toxin expression was verified by SDS-PAGE. For one-step purification Ni-NTA sepharose affinity chromatography was employed. For examination of purified toxin function, RBC hemolytic test was conducted. Results: The results showed that the FraC-coding gene was successfully cloned between NcoI and HindIII restriction sites and purified with affinity chromatography. Densitometric analysis represented the purity of approximately 97%. Hemolytic test indicated the purified FraC had remarkable lytic activity on RBC and almost lysed 50% of cells at the concentration value of 6.25 nM. Conclusion: The results indicated that not only purified toxin preserved its activity during expression and purification processes but also exerted its function at lower concentrations so that even the 0.09 nM displayed hemolytic effect.
https://ijbms.mums.ac.ir/article_8577_824c161b1816e4d3be8871c0d3bdfef3.pdf
2017-04-01
380
385
10.22038/ijbms.2017.8577
Fragaceatoxin C
Recombinant protein
Gene cloning
Hemolysis
Sea Anemone
Mehdi
Imani
m.imani@urmia.ac.ir
1
Department of Basic Sciences, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran
LEAD_AUTHOR
Hossein
Zarei Jaliani
zarei_sg@ibb.ut.ac.ir
2
Department of Genetics, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
AUTHOR
Mohammad Hassan
Kheirandish
3
Department of Genetics, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
AUTHOR
Mahnaz
Azadpour
mbiotecnology@gmail.com
4
Department of Genetics, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
AUTHOR
1. Anderluh G, Maček P. Cytolytic peptide and protein toxins from sea anemones (Anthozoa: Actiniaria). Toxicon 2002; 40:111-124.
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ORIGINAL_ARTICLE
The effects of gestational and lactational exposure to Nonylphenol on c-jun, and c-fos expression and learning and memory in hippocampus of male F1 rat
Objective(s): To investigate the effects of Nonylphenol (NP) in pups from dams exposed during gestational and lactational periods on immediate early genes (c-jun, c-fos) in hippocampus and the learning and memory of F1 rats. Materials and Methods: Twenty eight pregnant dams, stratified by pregnancy date, were randomly assigned into 4 groups, which were gavaged with NP at the doses of 50 mg/kg/day, 100 mg/kg/day, 200 mg/kg/day and groundnut oil, respectively. Step-down avoidance test, and learning and memory effects of NP were evaluated on 8-weeks-old pups. The expressions of c-jun and c-fos and the activities of choline acetyltransferase (ChAT) and acetylcholinesterase (AchE) were evaluated in hippocampus of pups. Results: Compared to the control, reaction time (RT) that pups spent to jump to the platform was longer (P=0.02), the number of errors were higher (P=0.01), and the step-down latency was shorter in the 200 mg/kg/day NP-treated group (P=0.04). Exposure to NP induced a significant reduction in ChAT activity in hippocampus in the 100 (P=0.005) and 200 mg/kg/day NP-treated groups (P=0.002), whereas exposure to 200 mg/kg/day caused a significant increase in AchE activity (P=0.004); a dose–response relationship was revealed between ChAT and AchE activities and NP exposure in the hippocampus of pups (r=-0.821, P=0.01; r=0.757, P=0.04). Exposure to NP in the 100 and 200 mg/kg/day NP-treated groups exhibited an increase in number of c-fos and c-jun positive cells. Conclusion: Exposure to NP might negatively affect learning and memory ability in F1 rats, possibly due to the alterations in the expression of c-jun and c-fos, and ChAT, AchE activities in hippocampus of pups.
https://ijbms.mums.ac.ir/article_8578_d37a05c44b6e1fe541166ec70bfd5c4a.pdf
2017-04-01
386
391
10.22038/ijbms.2017.8578
Learning and memory
Neurotransmitters Nonylphenol
Pups
Yu
Jie
1
School of Public Health, Zunyi Medical University, Zunyi Guizhou 563099, P.R. of China
AUTHOR
Wang
Pan
2
Department of Nuclear Medicine, The Affiliated Hospital of Zunyi Medical University, Zunyi Guizhou 563099, P.R. of China
AUTHOR
Yan
Wenxia
3
School of Public Health, Zunyi Medical University, Zunyi Guizhou 563099, P.R. of China
AUTHOR
Gao
Feng
4
School of Public Health, Zunyi Medical University, Zunyi Guizhou 563099, P.R. of China
AUTHOR
He
Liting
5
School of Public Health, Zunyi Medical University, Zunyi Guizhou 563099, P.R. of China
AUTHOR
Li
Wenmei
6
School of Public Health, Zunyi Medical University, Zunyi Guizhou 563099, P.R. of China
AUTHOR
Xu
Jie
xujie360@sina.com
7
School of Public Health, Zunyi Medical University, Zunyi Guizhou 563099, P.R. of China
LEAD_AUTHOR
1.Jie X, Yang W, Jie Y, Fan QY, Liu XY, Yan L, et al. Immune effects of nonylphenol on offspring of rats Exposed During Pregnancy. Hum Ecol Risk Assess 2010; 16:444–452.
1
2.Yu Jie, Fan QY, Binli H, Biao Z, Zheng F, Jianmei L, et al. Joint neurodevelopmental and behavioral effects of nonylphenol and estradiol on F(1) male rats. Int J Environ Heal R 2013; 23:321-330.
2
3.White R, Jobling S, Hoare S, Sumpter J, Parker M. Environmentally persistent alkylphenolic compounds are estrogenic. Endocrinology 2014; 135:175–182.
3
4.Perez-Cadahia B, Drobic B, Davie JR. Activation and function of immediate-early genes in the nervous system. Biochem Cell Biol 2011; 89:61–73.
4
5.Kubik S, Miyashita T, Guzowski JF. Using immediate-early genes to map hippocampal subregional functions. Learn Mem 2007; 14:758–770.
5
6.Jie X, Yang W, Jie Y, Hashim JH, Liu XY, Fan QY, et al. Toxic effect of gestational exposure to nonylphenol on F1 male rats. Birth Defects Res B Dev Reprod Toxicol 2010; 89:418–428.
6
7.Hollnagel JO, Ul Haq R, Behrens CJ, Maslarova A, Mody I, Heinemann U. No evidence for role of extracellular choline-acetyltransferase in generation of gamma oscillations in rat hippocampal slices in vitro. Neuroscience 2015; 284:459-469.
7
8.Uyanıkgil Y, Turgut M, Baka M. Effects of melatonin on the cerebellum of infant rat following kaolin-induced hydrocephalus: a histochemical and immunohistochemical study. Cerebellum 2017; 16:142-150.
8
9.Jie Y, Xuefeng Y, Mengxue Y, Xuesong Y, Jing Y, Yin T, et al. Mechanism of nonylphenol-induced neurotoxicity in F1 rats during sexual maturity. Wien Klin Wochenschr 2016; 128:426-434.
9
10.Thomas JD, La Fiette MH, Quinn VR, Riley EP. Neonatal choline supplementation ameliorates the effects of prenatal alcohol exposure on a discrimination learning task in rats. Neurotoxicol Teratol 2000; 22:703-711.
10
11.Vasilopoulou CG, Constantinou C, Giannakopoulou D, Giompres P, Margarity M. Effect of a1dult onset hypothyroidism on behavioral parameters and acetylcholinesterase isoforms activity in specific brain regions of male mice. Physiol Behav 2016; 164:284-291.
11
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13.Ludwig M, Tobin VA, Callahan MF, Papadaki E, Becker A, Engelmann M, et al. Intranasal application of vasopressin fails to elicit changes in brain immediate early gene expression, neural activity and behavioural performance of rats. J Neuroendocrinol 2013; 25:655-667.
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14.Herdegen T, Skene P, Bähr M. The c-Jun transcription factor–bipotential mediator of neuronal death, survival and regeneration. Trends Neurosci 1997; 20:227-231.
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15.Mirante O, Price M, Puentes W, Castillo X, Benakis C, Thevenet J, et al. Endogenous protease nexin-1 protects against cerebral ischemia. Int J Mol Sci 2013; 14:16719-16731.
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17
ORIGINAL_ARTICLE
Remyelination improvement after neurotrophic factors secreting cells transplantation in rat spinal cord injury
Objective(s): Neurotrophic factors secreting cells (NTS-SCs) may be a superior cell source for cell-based therapy in neurodegenerative diseases. NTS-SCs are able to secrete some neurotrophic Such as nerve growth factor and glia-derived neurotrophic factor. Our primary aim was to assess transplantation of neurotrophic factor secreting cells derived from human adipose-derived stem cells (hADSCs) into the damaged spinal cord rats and determine the potential of these cells in remyelination. Materials and Methods: To this end, 40 adult male Wistar rats were categorized into four groups including; control, lysolecithin (Lysophosphatidylcholines or LPC), vehicle, and NTS-SCs transplan-tation. Local demyelination was induced using LPC injection into the lateral column of spinal cord. Seven days after the lysolecithin lesion, the cells transplantation was performed. The ultrastructure of myelinated fibers was examined with a transmission electron microscope to determine the extent of myelin destruction and remyelinization 4 weeks post cell transplantation. Moreover, the presence of oligodendrocyte in the lesion of spinal cord was assessed by immunohistochemistry procedure. Results: The results of current study indicated that in NTF-SCs transplantation group, the remyelination process and the mean of myelin sheath thickness as well as axonal diameters were significantly higher than other groups (P<0.001). Furthermore, immunohistochemistry analysis revealed that in NTF-SCs transplantation group more than 10 percent of transplanted cells were positive for specific markers of oligodendrocyte cells. Conclusion: NTF-SCs transplantation represents a valuable option for cell-based therapy in the nervous tissue damages.
https://ijbms.mums.ac.ir/article_8580_a0ba8219c057d8eae4de0069f2468d07.pdf
2017-04-01
392
398
10.22038/ijbms.2017.8580
Lysolecithin lesion
Myelination
Neurotrophic factor-secreting cells (NTF-SCs)
Spinal cord injury
Shahnaz
Razavi
razavi@med.mui.ac.ir
1
Department of Anatomical Science, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
LEAD_AUTHOR
Nazem
Ghasemi
ghasemi_anatomy@yahoo.com
2
Department of Anatomical Science, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Mohammad
Mardani
mardani@med.mui.ac.ir
3
Department of Anatomical Science, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Hossein
Salehi
4
Department of Anatomical Science, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
1.Ng TK, Fortino VR, Pelaez D, Cheung HS. Progress of mesenchymal stem cell therapy for neural and retinal diseases. World J Stem Cells 2014; 6:111-119.
1
2.Yin F, Guo L, Meng CY, Liu YJ, Lu RF, Li P, et al. Transplantation of mesenchymal stem cells exerts anti-apoptotic effects in adult rats after spinal cord ischemia-reperfusion injury. Brain Res 2014; 1561:1-10.
2
3.Razavi S, Nazem G, Mardani M, Esfandiari E, Salehi H, Esfahani SH. Neurotrophic factors and their effects in the treatment of multiple sclerosis. Adv Biomed Res 2015; 4.
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4.Urschel BA, Hulsebosch CE. Schwann cell-neuronal interactions in the rat involve nerve growth factor. J Compa Neurol 1990; 296:114-122.
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5.Zhao T, Yan W, Xu K. Combined treatment with platelet-rich plasma and brain-derived neurotrophic factor-overexpressing bone marrow stromal cells supports axonal remyelination in a rat spinal cord hemi-section model. Cytotherapy 2013; 15:792-804.
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6.Someya Y, Koda M, Dezawa M. Reduction of cystic cavity, promotion of axonal regeneration and sparing, and functional recovery with transplanted bone marrow stromal cell-derived Schwann cells after contusion injury to the adult rat spinal cord: laboratory investigation. J Neurosurg Spine 2008;9: 600-610.
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7.Sen A, Lea-Currie YR, Sujkowska D. Adipogenic potential of human adipose derived stromal cells from multiple donors is heterogeneous. J Cell Biochem 2001; 81:312-319.
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8.Razavi S, Mardani M, Kazemi M. Effect of leukemia inhibitory factor on the myelinogenic ability of Schwann-like cells induced from human adipose-derived stem cells. Cell Mol Neurobiol 2013; 33:283-289.
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9.Decker L, Desmarquet-Trin-Dinh C, Taillebourg E, Ghislain J, Vallat JM, Charnay P. Peripheral myelin maintenance is a dynamic process requiring constant Krox20 expression. J Neurosci 2006; 26:9771-9779.
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10.Wei X, Du Z, Zhao L. IFATS collection: The conditioned media of adipose stromal cells protect against hypoxia-ischemia-induced brain damage in neonatal rats. Stem Cells 2009; 27:478-88.
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11.Jahn O, Tenzer S, Werner HB. Myelin proteomics: molecular anatomy of an insulating sheath. Mol Neurobiol 2009; 40:55-72.
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12.Tang L, Lu X, Zhu R. Adipose-derived stem cells expressing the neurogenin-2 promote functional recovery after spinal cord injury in rat. Cell Mol Neurobiol 2016; 36: 657-67.
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13.Hur JW, Cho TH, Park DH, Lee JB, Park JY, Chung YG. Intrathecal transplantation of autologous adipose-derived mesenchymal stem cells for treating spinal cord injury: A human trial. J Spinal Cord Med 2016 ; 39:655-664.
13
14.Razavi S, Razavi MR, Zarkesh Esfahani H, Kazemi M, Mostafavi FS. Comparing brain-derived neurotrophic factor and ciliary neurotrophic factor secretion of induced neurotrophic factor secreting cells from human adipose and bone marrow-derived stem cells. Dev Growth Differ 2013; 55:648-655.
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15.Sadan O, Shemesh N, Cohen Y, Melamed E, Offen D. Adult neurotrophic factor-secreting stem cells: a potential novel therapy for neurodegenerative diseases. Israel Med Assoc J IMAJ 2009; 11:201-204.
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16.Ghasemi N, Razavi S, Mardani M, Esfandiari E, Salehi H, Esfahani SH. Transplantation of human adipose-derived stem cells enhances remyelination in lysolecithin-induced focal demyelination of rat spinal cord. Mol Biotechnol 2014; 56:470-478.
16
17.Razavi S, Razavi MR, Kheirollahi-Kouhestani M, Mardani M, Mostafavi FS. Co-culture with neurotrophic factor secreting cells induced from adipose-derived stem cells: promotes neurogenic differentiation. Biochem Biophys Res Commun 2013; 440:381-387.
17
18.Razavi S, Razavi MR, Ahmadi N, Kazemi M. Estrogen treatment enhances neurogenic differentiation of human adipose derived stem cells in vitro. Iran J Basic Med Sci 2015; 18: 799-804.
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19.Boido M, Niapour A, Salehi H. Combined treatment by Co transplantation of mesenchymal stem cells and neural progenitors with exercise and enriched environment housing in mouse spinal cord injury. Adv Stem Cells 2014; 22.
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20.Karimi-Abdolrezaee S, Billakanti R. Reactive astrogliosis after spinal cord injury—beneficial and detrimental effects. Mol Neurobiol 2012; 46:251-264.
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21.Kim BG, Hwang DH, Lee SI, Kim EJ, Kim SU. Stem cell-based cell therapy for spinal cord injury. Cell Transplant 2007; 16:355-364.
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22.Zurita M, Vaquero J. Bone marrow stromal cells can achieve cure of chronic paraplegic rats: functional and morphological outcome one year after transplantation. Neurosci Lett 2006; 402:51-56.
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23.Kulbatski I, Mothe AJ, Keating A, Hakamata Y, Kobayashi E, Tator CH. Oligodendrocytes and radial glia derived from adult rat spinal cord progenitors: morphological and immunocytochemical charac-terization. J Histochem Cytochem 2007; 55:209-222.
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24.Pisati F, Bossolasco P, Meregalli M. Induction of neurotrophin expression via human adult mesenchymal stem cells: implication for cell therapy in neurodegenerative diseases. Cell Transplant 2007; 16:41-55.
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25.Wang H, Wang Y, Li D. VEGF inhibits the inflammation in spinal cord injury through activation of autophagy. Biochem Biophys Res Commun 2015; 464:453-458.
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26. Abbaszadeh HA, Tiraihi T, Noori-Zadeh A, Delshad AR, Sadeghizade M, Taheri T. Human ciliary neurotrophic factor–overexpressing stable bone marrow stromal cells in the treatment of a rat model of traumatic spinal cord injury. Cytotherapy 2015; 17:912-921.
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27. Kovalchuk Y, Holthoff K, Konnerth A. Neurotrophin action on a rapid timescale. Curr Neurobiol 2004;14:558-563.
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28.Zhang H, Wu F, Kong X. Nerve growth factor improves functional recovery by inhibiting endoplasmic reticulum stress-induced neuronal apoptosis in rats with spinal cord injury. J Translat Med 2014;12:1.
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29.Harvey AR, Lovett SJ, Majda BT, Yoon JH, Wheeler LP, Hodgetts SI. Neurotrophic factors for spinal cord repair: Which, where, how and when to apply, and for what period of time? Brain Res 2015; 1619:36-71.
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30. Sadan O, Melamed E, Offen D. Intrastriatal transplantation of neurotrophic factor-secreting human mesenchymal stem cells improves motor function and extends survival in R6/2 transgenic mouse model for Huntington’s disease. PLOS Curr 2012; 4:e4f7f6dc013d4e.
30
31. Sadan O, Shemesh N, Barzilay R, Bahat-Stromza M, Melamed E, Cohen Y, et al. Migration of neurotrophic factors-secreting mesenchymal stem cells toward a quinolinic acid lesion as viewed by magnetic resonance imaging. Stem Cells 2008; 26:2542-2551.
31
ORIGINAL_ARTICLE
Therapeutic effects of ellagic acid on memory, hippocampus electrophysiology deficits, and elevated TNF-α level in brain due to experimental traumatic brain injury
Objective(s): Cognitive defects such as learning and memory impairment are amongst the most repetitious sequelae after sever and moderate traumatic brain injury (TBI). It was suggested that ellagic acid (EA), an innate phenol product, display neuroprotective properties against oxidative and inflammatory damages after brain injury. The object of the current study was therapeutic properties of EA on blood-brain barrier (BBB) interruption and elevated content of TNF-α in brain tissue followed by neurologic aftereffects, cognitive and brain electrophysiology deficits as outcomes of diffuse TBI in rat. Materials and Methods: TBI was induced by a 200 g weight falling by a 2-m height through a free-falling tube onto the head of anesthetized rat. TBI rats treated immediately after trauma with EA (100 mg/kg, IP) once every 8 hr until 48 hr later. Neurologic outcomes, passive avoidance task (PAT), hippocampal long-term potentiation (LTP), BBB permeability and content of TNF-α in brain tissue were evaluated. Results: TBI induced significant impairments in neurological score, BBB function, PAT and hippocampal LTP in TBI+Veh group in compare with Sham+Veh (P<0.001). EA treatment decreased neurologic severity score (NSS), restored increased BBB permeability, cognitive and hippocampal LTP abnormalities, and elevated brain content of TNF-α due to TBI significantly (P<0.001). Conclusion: Our findings propose that EA can restore NSS, cognitive and LTP deficits and prevent brain inflammation may by restore BBB permeability as well as lowering brain content of TNF-α following TBI.
https://ijbms.mums.ac.ir/article_8581_6ed03decf4cbf55987e5a252bb90ce5c.pdf
2017-04-01
399
407
10.22038/ijbms.2017.8581
Blood-brain barrier
Ellagic acid
LTP
Memory
TNF-α
Traumatic brain injury
Shahram
Mashhadizadeh
mashhadizadeh79@yahoo.com
1
Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran
AUTHOR
Yaghoub
Farbood
2
Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran
AUTHOR
Mahin
Dianat
3
Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran
AUTHOR
Ali
Khodadadi
akhodaddadi@gmail.com
4
Department of Immunology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran
AUTHOR
Alireza
Sarkaki
sarkaki_@ajums.ac.ir
5
Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran
LEAD_AUTHOR
1. Al Nimer F, Lindblom R, Ström M, Guerreiro-Cacais AO, Parsa R, Aeinehband S, et al. Strain influences on inflammatory pathway activation, cell infiltration and complement cascade after traumatic brain injury in the rat. Brain Behav Immun 2013; 27:109-122.
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4.Kumar A, Loane D. Neuroinflammation after traumatic brain injury: opportunities for therapeutic intervention. Brain Behav Immun 2012; 26:1191-1201.
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71
ORIGINAL_ARTICLE
Naringin enhances osteogenic differentiation through the activation of ERK signaling in human bone marrow mesenchymal stem cells
Objective(s): Naringin has been reported to regulate bone metabolism. However, its effect on osteogenesis remains unclear. The aim was to investigate the effect of naringin on osteogenic differentiation of human bone marrow mesenchymal stem cells (hBMSCs) through the activation of the ERK signaling pathway in osteogenic differentiation. Materials and Methods: Annexin V-FITC assay and MTT assay were used to measure the effect of naringin on cytotoxicity and proliferation of hBMSCs, respectively. Alkaline phosphatase activity analysis, Alizarin Red S staining, Western blotting, and real-time PCR assay were used to evaluate both the potential effect of naringin on osteogenic differentiation and the role of ERK signaling pathway in osteogenic differentiation. Results: Our results showed that naringin had no obvious toxicity on hBMSCs, and could significantly promote the proliferation of hBMSCs. Naringin also enhanced the osteogenic differentiation of hBMSCs and increased the protein and mRNA expression levels of osteogenic markers such as Runx-2, OXS, OCN, and Col1 in a dose-dependent manner. In addition, we found that the enhancing effect of naringin on osteogenic differentiation was related to the activation of phosphor-ERK, with an increase in duration of activity from 30 min to 120 min. More importantly, both the enhancing effect of naringin on osteogenic differentiation and the activity effect of naringin on ERK signaling pathway were reversed by U0126 addition. Conclusion: Our findings demonstrated that naringin promoted proliferation and osteogenesis of hBMSCs by activating the ERK signaling pathway and it might be a potential therapeutic agent for treating or preventing osteoporosis.
https://ijbms.mums.ac.ir/article_8582_6b7710b5fdcf2a72cd93ad05e39cc426.pdf
2017-04-01
408
414
10.22038/ijbms.2017.8582
Bone marrow-mesenchymal stem cells
ERK signaling pathway
Naringin
Osteogenic differentiation
Huichao
Wang
henanhuichao@126.com
1
Luoyang Orthopedic Hospital of Henan Province, Orthopedic Institute of Henan Province, Luoyang 471002, China
AUTHOR
Chunbo
Li
lichunbo142@126.com
2
Shanghai First Maternity and Infant Hospital, Tongji University of Medicine. Shanghai, 200126, China
AUTHOR
Jianming
Li
jianmingll@sina.com
3
Luoyang Orthopedic Hospital of Henan Province, Orthopedic Institute of Henan Province, Luoyang 471002, China
AUTHOR
Yingjie
Zhu
874569077@qq.com
4
Luoyang Orthopedic Hospital of Henan Province, Orthopedic Institute of Henan Province, Luoyang 471002, China
AUTHOR
Yudong
Jia
5
Luoyang Orthopedic Hospital of Henan Province, Orthopedic Institute of Henan Province, Luoyang 471002, China
AUTHOR
Ying
Zhang
yingzi401533@163.com
6
Luoyang Orthopedic Hospital of Henan Province, Orthopedic Institute of Henan Province, Luoyang 471002, China
AUTHOR
Xiaodong
Zhang
xdzhangzh@163.com
7
Luoyang Orthopedic Hospital of Henan Province, Orthopedic Institute of Henan Province, Luoyang 471002, China
AUTHOR
Wenlong
Li
8
Henan University of Traditional Chinese Medicine, Henan Province, Zhengzhou 450000, China
AUTHOR
Lei
Cui
leicuimd@yahoo.cn
9
Medical Science & Research Center, Beijing Shijitan Hospital Affiliated to Capital Medical University, 10 Tieyi Road, Beijing 100038, China
AUTHOR
Wuyin
Li
lwy6507@163.com
10
Luoyang Orthopedic Hospital of Henan Province, Orthopedic Institute of Henan Province, Luoyang 471002, China
AUTHOR
Youwen
Liu
liuyouwen543@sina.com
11
Luoyang Orthopedic Hospital of Henan Province, Orthopedic Institute of Henan Province, Luoyang 471002, China
LEAD_AUTHOR
1.Makras P, Delaroudis S, Anastasilakis AD. Novel therapies for osteoporosis. Metabolism 2015; 64:1199-1214.
1
2.Drake MT, Clarke BL, Lewiecki EM. The Pathophysiology and Treatment of Osteoporosis. Clin Ther 2015; 37:1837-1850.
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3.Lim SY, Bolster MB. Current approaches to osteoporosis treatment. Curr Opin Rheumatol 2015; 27:216-224.
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4.James AW. Review of Signaling Pathways Governing MSC Osteogenic and Adipogenic Differentiation. Scientifica 2013; 2013:684736.
4
5.Bidwell JP, Alvarez MB, Hood M, Jr., Childress P. Functional impairment of bone formation in the pathogenesis of osteoporosis: the bone marrow regenerative competence. Curr Osteoporos Rep 2013; 11:117-125.
5
6.Guan M, Yao W, Liu R, Lam KS, Nolta J, Jia J, et al. Directing mesenchymal stem cells to bone to augment bone formation and increase bone mass. Nat Med 2012; 18:456-462.
6
7.McArthur GA. Combination Therapies to Inhibit the RAF/MEK/ERK Pathway in Melanoma: We are not Done Yet. Front Oncol 2015; 5:161.
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8.Ying X, Cheng S, Wang W, Lin Z, Chen Q, Zhang W, et al. Effect of lactoferrin on osteogenic differentiation of human adipose stem cells. Int Orthop 2012; 36:647-653.
8
9.Gonzalez-Andrades MG, I., Alaminos M. Advances in the Field of Tissue Engineering and Regenerative Medicine: State of the Art and Regulatory Issues. J Biomater Tissue Eng 2013; 3:245-260.
9
10.Li Y, Wang J, Chen G, Feng S, Wang P, Zhu X, et al. Quercetin promotes the osteogenic differentiation of rat mesenchymal stem cells via mitogen-activated protein kinase signaling. Exp Ther Med 2015; 9:2072-2080.
10
11.Zhou C, Zhang X, Xu L, Wu T, Cui L, Xu D. Taurine promotes human mesenchymal stem cells to differentiate into osteoblast through the ERK pathway. Amino Acids 2014; 46:1673-1680.
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12.Xu D, Xu L, Zhou C, Lee WY, Wu T, Cui L, et al. Salvianolic acid B promotes osteogenesis of human mesenchymal stem cells through activating ERK signaling pathway. Int J Biochem Cell Biol 2014; 51:1-9.
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13.Kim JM, Lee JE, Ryu SH, Suh PG. Chlormadinone acetate promotes osteoblast differentiation of human mesenchymal stem cells through the ERK signaling pathway. Euro J Pharmacol 2014; 726:1-8.
13
14.Bharti S, Rani N, Krishnamurthy B, Arya DS.
14
Preclinical evidence for the pharmacological actions of naringin: a review. Planta Med 2014; 80:437-451.
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15.Li F, Sun X, Ma J, Ma X, Zhao B, Zhang Y, et al. Naringin prevents ovariectomy-induced osteoporosis and promotes osteoclasts apoptosis through the mitochondria-mediated apoptosis pathway. Biochem Biophys Res Commun 2014; 452:629-635.
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18.Baharara J, Amini E, Kerachian MA, Soltani M. The osteogenic differentiation stimulating activity of Sea cucumber methanolic crude extraction on rat bone marrow mesenchymal stem cells. Iran J Basic Med Sci 2014; 17:626-631.
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20. Hou X, Shen Y, Zhang C, Zhang L, Qin Y, Yu Y, et al. A specific oligodeoxynucleotide promotes the differentiation of osteoblasts via ERK and p38 MAPK pathways. Int J Mol Sci 2012; 13:7902-7914.
21
21. Jagetia GC, Reddy TK, Venkatesha VA, Kedlaya R. Influence of naringin on ferric iron induced oxidative damage in vitro. Clin Chim Acta 2004; 347:189-197.
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23
23.Pang WY, Wang XL, Mok SK, Lai WP, Chow HK, Leung PC, et al. Naringin improves bone properties in ovariectomized mice and exerts oestrogen-like activities in rat osteoblast-like (UMR-106) cells. Br J Pharmacol 2010; 159:1693-1703.
24
24.Li L, Zeng Z, Cai G. Comparison of neoeriocitrin and naringin on proliferation and osteogenic differentiation in MC3T3-E1. Phytomedicine 2011; 18:985-989.
25
25.Liu M, Li Y, Yang ST. Effects of naringin on the proliferation and osteogenic differentiation of human amniotic fluid-derived stem cells. J Tissue Eng Regen Med 2014:doi: 10.1002/term.1911.
26
26.Komori T, Yagi H, Nomura S, Yamaguchi A, Sasaki K, Deguchi K, et al. Targeted disruption of Cbfa1 results in a complete lack of bone formation owing to maturational arrest of osteoblasts. Cell 1997; 89:755-764.
27
27.Potier E, Noailly J, Ito K. Directing Bone marrow-derived stromal cell function with mechanics. J Biomech 2010;43:807-817.
28
28. Miraoui H, Oudina K, Petite H, Tanimoto Y, Moriyama K, Marie PJ. Fibroblast growth factor receptor 2 promotes osteogenic differentiation in mesenchymal cells via ERK1/2 and protein kinase C signaling. J Biol Chem 2009; 284:4897-4904.
29
29.Xu C, Zheng Z, Fang L, Zhao N, Lin Z, Liang T, et al. Phosphatidylserine enhances osteogenic differentiation in human mesenchymal stem cells via ERK signal pathways. Mater Sci Eng C Mater Biol Appl 2013; 33:1783-1788.
30
ORIGINAL_ARTICLE
Antimalarial evaluation of selected medicinal plant extracts used in Iranian traditional medicine
Objective(s): In an attempt to discover new natural active extracts against malaria parasites, the present study evaluated the antiplasmodial properties of selected plants based on Iranian traditional medicine. Materials and Methods: Ten plant species found in Iran were selected and collected based on the available literature about the Iranian traditional medicine. The methanolic extracts of these plants were investigated for in vitro antimalarial properties against chloroquine-sensitive (3D7) and multi-drug resistant (K1) strains of Plasmodium falciparum. Their in vivo activity against Plasmodium berghei infection in mice was also determined. Cytotoxicity tests were carried out using the Raji cells line using the MTT assay. The extracts were phytochemically screened for their active constituents. Results: According to the IC50 and selectivity index (SI) values, of the 10 selected plant species, Citrullus colocynthis, Physalis alkekengi, and Solanum nigrum displayed potent in vitro antimalarial activity against both 3D7 and K1 strains with no toxicity (IC50= 2.01-18.67 µg/ml and SI=3.55 to 19.25). Comparisons between treated and untreated control mice showed that the mentioned plant species reduced parasitemia by 65.08%, 57.97%, and 60.68%, respectively. The existence of antiplasmodial compounds was detected in these plant extracts. Conclusion: This was the first study to highlight the in vitro and in vivo antiplasmodial effects of C. colocynthis, P. alkekengi, and S. nigrum in Iran. Future studies can use these findings to design further biological tests to identify the active constituents of the mentioned plant species and clarify their mechanism of action.
https://ijbms.mums.ac.ir/article_8583_83cc6911df149ba2a970738ac2cef15a.pdf
2017-04-01
415
422
10.22038/ijbms.2017.8583
Antimalarials
Cytotoxicity
Phytochemicals
Plasmodium falciparum
Traditional Medicine
Mohammad Hossein
Feiz Haddad
hfeizhaddad@yahoo.com
1
Infectious and Tropical Diseases Research Center, Health Research Institute Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
LEAD_AUTHOR
Hamidreza
Mahbodfar
2
Department of Parasitology, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
AUTHOR
Zahra
Zamani
zamani@pasteur.ac.ir
3
Department of Biochemistry, Pasteur Institute of Iran, Tehran, Iran
AUTHOR
Ali
Ramazani
mavara_hr@yahoo.com
4
Zanjan Pharmaceutical Biotechnology Research Center, Zanjan University of Medical Sciences, Zanjan, Iran
AUTHOR
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55
ORIGINAL_ARTICLE
Effect of genistein on expression of pancreatic SIRT1, inflammatory cytokines and histological changes in ovariectomized diabetic rat
Objective(s): Genistein is reported to have anti-diabetic and anti-inflammatory functions, in particular, direct effects on β-cell proliferation and insulin secretion. In this study, we investigated the anti-inflammatory effect of genistein on the pancreatic β-cells in ovariectomized diabetic rat. Materials and Methods:Forty female rats were divided into four groups: sham, bilateral ovariectomy (OVX), OVX.D (OVX+diabetes) and OVX.D.G (OVX.D+genistein). After bilateral ovariectomy, rats in the diabetic groups were fed high-fat diet (HFD), ad libitum for 4 weeks, and then a low dose of streptozotocin (STZ) (30 mg/kg) injected intraperitoneally. Genistein (1 mg/kg/day; SC) was administrated for 8 weeks. At the end of 8 weeks, pancreas tissue was removed and used for western blotting and Hematoxylin-Eosin staining. Results: Treatment with genistein declined inflammation and tissue injury, and this decline was correlated with the expression of SIRT1. OVX and OVX.D significantly increased Nf-кB and IL-1β expression and decreased SIRT1 levels compared to sham group (P<0.05). Significant reduction of Nf-кB and IL-1β, and increasing of SIRT1 were observed during genistein treatment (P<0.05). Conclusion: Estrogen deficiency alone or with HFD increased pancreatic inflammation. However, subcutaneous administration of gtenistein prevented from these inflammatory changes in the pancreas of a surgery animal model of ovariectomy with or without diabetes. Our results support the potential preventing effect of genistein from pancreatic injury.
https://ijbms.mums.ac.ir/article_8585_7f7493ee63a8324631016b4c678fa836.pdf
2017-04-01
423
429
10.22038/ijbms.2017.8585
Diabetes
Genistein
Inflammatory cytokines-ovariectomy
SIRT1
Hadi
Yousefi
1
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Alireza
Alihemmati
hemmati@yahoo.com
2
Department of Histology & Embryology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Pouran
Karimi
3
Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Mohammad Reza
Alipour
alipourmr52@yahoo.com
4
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Parisa
Habibi
dr.habibi2007@yahoo.com
5
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Nasser
Ahmadiasl
n.ahmadiacl@gmail.com
6
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
LEAD_AUTHOR
1. Arnush M, Heitmeier MR, Scarim AL, Marino MH, Manning PT, Corbett JA. IL-1 produced and released endogenously within human islets inhibits beta cell function. J Clin Invest 1998; 102:516.
1
2. Corbett JA, McDaniel ML. Intraislet release of interleukin 1 inhibits beta cell function by inducing beta cell expression of inducible nitric oxide synthase. J Exp Med 1995; 181:559-568.
2
3. Pfeilschifter J, Köditz R, Pfohl M, Schatz H. Changes in proinflammatory cytokine activity after menopause. Endocr Rev 2002; 23:90-119.
3
4. Eizirik DL, Colli ML, Ortis F. The role of inflammation in insulitis and β-cell loss in type 1 diabetes. Nat Rev Endocrinol 2009; 5:219-226.
4
5. Ortis F, Miani M, Colli M, Cunha D, Gurzov E, Allagnat F, et al. Differential usage of NF-κB activating signals by IL-1β and TNF-α in pancreatic beta cells. FEBS Lett 2012; 586:984-989.
5
6. Lee JH, Song MY, Song EK, Kim EK, Moon WS, Han MK, et al. Overexpression of SIRT1 protects pancreatic β-cells against cytokine toxicity by suppressing the nuclear factor-κB signaling pathway. Diabetes 2009; 58:344-351.
6
7. Glazier MG, Bowman MA. A review of the evidence for the use of phytoestrogens as a replacement for traditional estrogen replacement therapy. Arch Inter Med 2001; 161:1161-1172.
7
8. Gilbert ER, Liu D. Anti-diabetic functions of soy isoflavone genistein: mechanisms underlying its effects on pancreatic β-cell function. Food Funct 2013; 4:200-212.
8
9. Byun EB, Sung NY, Yang MS, Lee BS, Song DS, Park JN, et al. Anti-inflammatory effect of gamma-irradiated genistein through inhibition of NF-κB and MAPK signaling pathway in lipopolysaccharide-induced macrophages. Food Chem Toxicol 2014; 74:255-264.
9
10. Irigoyen MC, Paulini J, Flores LJ, Flues K, Bertagnolli M, Moreira ED, et al. Exercise training improves baroreflex sensitivity associated with oxidative stress reduction in ovariectomized rats. Hypertension 2005; 46:998-1003.
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11. Srinivasan K, Ramarao P. Animal models in type 2 diabetes research: an overview. Indian J Med Res 2007; 125:451.
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12. Su X, Meng X, Sun C, Liu L, Su B. Intramuscular injection of soluble receptor for advanced glycation endproducts expression vector prevents the development of streptozotocin‐induced diabetes mellitus in rats on high fat diet. J Diabetes 2011; 3:309-316.
12
13. Habibi P, Alihemmati A, NourAzar A, Yousefi H, Mortazavi S, Ahmadiasl N. Expression of the Mir-133 and Bcl-2 could be affected by swimming training in the heart of ovariectomized rats. Iran J Basic Med Sci 2016; 19:381-387.
13
14. Dosi R, Bhatt N, Shah P, Patell R. Cardiovascular disease and menopause. J Clin Diagn Res 2014; 8:62.
14
15. Kim C, Edelstein SL, Crandall JP, Dabelea D, Kitabchi AE, Hamman RF, et al. Menopause and risk of diabetes in the Diabetes Prevention Program. Menopause 2011;18:857-868.
15
16. Choi SB, Jang JS, Park S. Estrogen and exercise may enhance β-cell function and mass via insulin receptor substrate 2 induction in ovariectomized diabetic rats. Endocrinology 2005; 146:4786-4794.
16
17. Donath MY, Böni-Schnetzler M, Ellingsgaard H, Ehses JA. Islet inflammation impairs the pancreatic β-cell in type 2 diabetes. Physiology 2009; 24:325-331.
17
18. Kim HK, Nelson-Dooley C, Della-Fera MA, Yang JY, Zhang W, Duan J, et al. Genistein decreases food intake, body weight, and fat pad weight and causes adipose tissue apoptosis in ovariectomized female mice. J Nutr 2006; 136:409-414.
18
19. El-Kordy EA, Alshahrani AM. Effect of genistein, a natural soy isoflavone, on pancreatic β-Cells of streptozotocin-induced diabetic rats: histological and immunohistochemical study. J Microsc Ultrastruct 2015; 3:108-119.
19
20. Habibi P, Alihemmati A, Nasirzadeh M, Yousefi H, Habibi M, Ahmadiasl N. Involvement of microRNA-133 and-29 in cardiac disturbances in diabetic ovariectomized rats. Iranian J Basic Med Sci 2016; 19:1177.
20
21. Lee HJ, Hong YS, Yang SJ. Interaction between NLRP3 inflammasome and Sirt1/6: metabolomics approach. FASEB J 2015; 29:913.
21
22. Amoli MM, Larijani B. Would blockage of cytokines improve the outcome of pancreatic islet transplantation? Med Hypotheses 2006; 66:816-819.
22
23. Aharon-Hananel G, Jörns A, Lenzen S, Raz I, Weksler-Zangen S. Antidiabetic effect of interleukin-1β antibody therapy through β-Cell protection in the cohen diabetes-sensitive rat. Diabetes 2015; 64:1780-1785.
23
24. Gao X, Liu K, Huang F, Zhang D, Guo X, Wang M, et al. Positive and negative regulation of insulin action by genistein in the endothelium. J Nutr Biochem 2013; 24:222-230.
24
25. Hirasaka K, Maeda T, Ikeda C, Haruna M, Kohno S, Abe T, et al. Isoflavones derived from soy beans prevent MuRF1-mediated muscle atrophy in C2C12 myotubes through SIRT1 activation. J Nutr Sci Vitaminol 2013; 59:317-324.
25
26. Kim EK, Kwon KB, Song MY, Seo SW, Park SJ, Ka SO, et al. Genistein protects pancreatic β cells against cytokine-mediated toxicity. Mol Cell Endocrinol 2007; 278:18-28.
26
ORIGINAL_ARTICLE
Novel derivatives of phthalimide with potent anticonvulsant activity in PTZ and MES seizure models
Objective(s): Phthalimide-based derivatives have anticonvulsant activity like as phenytoin by inhibition of sodium channel. In our previously research we mentioned about some phthalimide derivatives as potent anticonvulsant agents. Materials and Methods: Fourteen analogs of 2-substituted phthalimide pharmacophore were synthesized and then were evaluated for the anticonvulsant activities in pentylenetetrazole-induced seizures (PTZ) and maximal electroshock seizure (MES) models. Results: The in vivo screening results showed that all the analogs have the ability to protect against the maximal electroshock and PTZ. The compounds 3 and 9 elevated clonic seizure thresholds at 30 min which were more active than the standard medicine phenytoin. Compounds 3, 6, 7, 11, 13 and 14 with 100% protection were the most potent ones in tonic seizure. The most potent compound in the both PTZ and MES models was compound 3. Using a model of the open pore of sodium channel, all of the compounds were docked. Results of docking showed that the ligands interacted mainly with residues II-S6 of NaV1.2 by making hydrogen bonds and have additional hydrophobic interactions with other domains in the channel's inner pore. Conclusion: Some of these compounds are more potent than phenytoin simultaneously in the clonic and tonic seizures.
https://ijbms.mums.ac.ir/article_8586_09ccb430c0f02e1c24ea319f9072bb44.pdf
2017-04-01
430
437
10.22038/ijbms.2017.8586
Anticonvulsant
Docking
MES seizure
Phthalimide
PTZ seizure
Sodium channel
Asghar
Davood
adavood2001@yahoo.com
1
Department of Medicinal Chemistry, Faculty of Pharmacy, Pharmaceutical Sciences Branch, Islamic Azad University, Tehran, Iran
LEAD_AUTHOR
Maryam
Iman
iman1359@yahoo.com
2
Department of Pharmaceutics, Faculty of pharmacy, Baqiyatallah University of Medical Sciences, Tehran, Iran
AUTHOR
Hanieh
Pouriaiee
poriaee@yahoo.com
3
Department of Pharmacology and Toxicology, Pharmaceutical Sciences Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Hamed
Shafaroodi
shafaroodi@yahoo.com
4
Department of Pharmacology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Sepideh
Akhbari
5
Department of Medicinal Chemistry, Faculty of Pharmacy, Pharmaceutical Sciences Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Leila
Azimidoost
azimidost@yahoo.com
6
Department of Medicinal Chemistry, Faculty of Pharmacy, Pharmaceutical Sciences Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Erfan
Imani
imani@yahoo.com
7
Department of Medicinal Chemistry, Faculty of Pharmacy, Pharmaceutical Sciences Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Somaieh
Rahmatpour
rahmatpour@yahoo.com
8
Department of Medicinal Chemistry, Faculty of Pharmacy, Pharmaceutical Sciences Branch, Islamic Azad University, Tehran, Iran
AUTHOR
1.Donner EJ, Snead OC. New generation anticonvulsants for the treatment of epilepsy in children. Neuro RX 2006; 3:170–180.
1
2.Stefan H, Feuerstein T. Novel anticonvulsant drugs. Pharmacol Therap 2007; 113:165-183.
2
3.Brodie MJ. Antiepileptic drug therapy the story so far. Seizure 2010; 19:650–655.
3
4.Lacoste L, Bartolucci S, Lapointey J. Pentylenetetrazole inhibits glutamate dehydrogenase and aspartate aminotransferase, and stimulates GABA aminotransferase in homogenates from rat cerebral cortex. Can J Physiol Pharmacol 1988; 66:1135–1138.
4
5.Wang Y, Jones PJ, Batts TW, Landry V, Patel MK, Brown ML. Ligand-based design and synthesis of novel sodium channel blockers from a combined phenytoin–lidocaine pharmacophore. Bioorg Med Chem 2009; 17:7064–7072.
5
6.Catterall WA, Goldin AL, Waxman SG. International union of pharmacology. XLVII. Nomenclature and structure-function relationships of voltage-gated sodium channels. Pharmacol Rev 2005; 57:397–409.
6
7.Goldin AL. Resurgence of sodium channel research. Annu Rev Physiol 2001; 63: 871.
7
8.Vamecq J, Bac P, Herrenknecht C, Maurois P, Delcourt P, Stables JP. Synthesis and anticonvulsant and neurotoxic properties of substituted N-Phenyl derivatives of the phthalimide pharmacophore. J Med Chem 2000; 43:1311-1319.
8
9.Małgorzata W, Katarzyna KK. Synthesis and Anticonvulsant Evaluation of Some N-Substituted Phthalimides. Acta Poloniae Pharmaceutica Drug Res 2009; 66:249-257.
9
10.Davood A, Shafaroodi H, Amini M, Nematollahi A, Shirazi M, Iman M. Design, Synthesis and protection against pentylenetetrazole-induced seizure of N-aryl derivatives of the phthalimide pharmacophore. Med Chem 2012; 8:953-963.
10
11.Davood A, Amini M, Azimidoost L, Rahmatpour S, Nikbakht A, Iman, M, et al. Docking, synthesis, and pharmacological evaluation of isoindoline derivatives as anticonvulsant agents. Med Chem Res 2013; 22:3177-3184.
11
12.Iman M, Saadabadi A, Davood A. Docking Studies of Phthalimide Pharmacophore as a Sodium Channel Blocker. Iran J Basic Med Sci 2013; 16:1016-1021.
12
13.Shafaroodi H, Moezi L, Fakhrzad A, Hassanipour M, Rezayat M, Dehpour AR. The involvement of nitric oxide in the anti-seizure effect of acute atorvastatin treatment in mice. Neurosci Res 2012; 34:847-853.
13
ORIGINAL_ARTICLE
Protective effect of bioactive compounds from Echinophora cinerea against cisplatin-induced oxidative stress and apoptosis in the PC12 cell line
Objective(s): The present study aims to evaluate the protective effect of the compounds isolated from Echinophora cinerea (E. cinerea) against oxidative stress and apoptosis induced by cisplatin (CIS) in PC12 cells. Materials and Methods: Six compounds were isolated as quercetrin-3-O-β-D-glucopyranoside (QUE), osthol (OST), verbenone-5-O-β-D-glycopyranoside (VER), Isoimperatorin (ISO), kaempferol-3-O-β-D-glucopyranoside (KAM), and echinophorin B (ECH). For this study, we used MTT reduction assay for detection of protective effects of isolated compounds on CIS-induced cytotoxicity in PC12 cells. The effects of isolated compounds against apoptosis induced by CIS were investigated through the measurement of mitochondrial membrane potential (MMP), Bax and Bcl2 mRNA expression, and caspase-3 activation. We also assessed oxidative stress by measuring reactive oxygen species (ROS) generation with 2′, 7′-dichlorofluorescein diacetate (DCFH-DA). Results: Treatment of cells with QUE and OST before exposure to the CIS increased cell viability, i.e., these compounds protected the cells against CIS -induced cytotoxicity. In addition, pre-treatment with QUE and OST decreased CIS-induced apoptosis through up-regulation of Bcl-2, inhibition of caspase-3 activity, and mitochondrial membrane potential (MMP) increase. OST decreased ROS generation induced by CIS, as well. Conclusion: Our in vitro experiment showed that QUE and OST are apoptotic inhibitors that effectively block CIS-induced neurotoxicity predicting their therapeutic potential in the prevention of chemotherapy-induced neurotoxicity.
https://ijbms.mums.ac.ir/article_8587_4dcb4679137cdec65a73c5fa1f7491c0.pdf
2017-04-01
438
445
10.22038/ijbms.2017.8587
Apoptosis
Cisplatin
Echinophora cinerea
Neuroprotection
Osthole
Quercetin
Yald
Shokoohinia
1
Pharmaceutical Sciences Research Center, School of Pharmacy, Kermanshah University of Medical Sciences, Kermanshah, Iran
AUTHOR
Shekoufeh
Khajouei
2
Pharmaceutical Sciences Research Center, School of Pharmacy, Kermanshah University of Medical Sciences, Kermanshah, Iran
AUTHOR
Farahnaz
Ahmadi
ahmadif32@yahoo.com
3
Pharmaceutical Sciences Research Center, School of Pharmacy, Kermanshah University of Medical Sciences, Kermanshah, Iran
AUTHOR
Nastaran
Ghiasvand
4
Student Research Committee, School of Pharmacy, Kermanshah University of Medical Sciences, Kermanshah, Iran
AUTHOR
Leila
Hosseinzadeh
l_hoseinzadeh@yahoo.com
5
Pharmaceutical Sciences Research Center, School of Pharmacy, Kermanshah University of Medical Sciences, Kermanshah, Iran
LEAD_AUTHOR
1. Gulec M,Oral E, Dursun OB,Yucel A,Hacimuftuoglu A,Akcay F. Mirtazapine protects against cisplatin‐induced oxidative stress and DNA damage in the rat brain. Physical CiNeuro Sci 2013;67 : 50-8.
1
2. Cavaletti G , PezzoniG, Pisano C, Oggioni N, Sala, F, Zoia C. Cisplatin-induced peripheral neurotoxicity in rats reduces the circulating levels of nerve growth factor. Neuro Sci Lett 2002;322:103-106.
2
3. Podratz JL,Knight AM, Ta LE,Staff NP, Gass JM, GenelinK. Cisplatin induced mitochondrial DNA damage in dorsal root ganglion neurons. Neuro Biol Dis 2011;41: 661-668.
3
4. Park SA,Choi KS,Bang JH, Huh K, Kim SU. Cisplatin‐Induced Apoptotic Cell Death in Mouse Hybrid Neurons Is Blocked by Antioxidants Through Suppression of Cisplatin‐Mediated Accumulation of p53 but Not of Fas/Fas Ligand. J Neuro Chem 2000;75 : 946-953.
4
5. da Silva Machado C, Mendonca LM, de Paula Venancio V,Bianchi MLP, Antunes, LMG. Coenzyme Q10 protects Pc12 cells from cisplatin-induced DNA damage and neurotoxicity. Neuro Toxicol 2013;36:10-16.
5
6. Karimi G, Ramezani M, Tahoonian Z, Cisplatin nephrotoxicity and protection by milk thistle extract in rats. Evid-BasComplementary Alt Med 2005; 2:383-386.
6
7. Shokoohinia Y, Hosseinzadeh L, Moieni-Arya M, Mostafaie A, Mohammadi-Motlagh, H-R. Osthole Attenuates Doxorubicin-Induced Apoptosis in PC12 Cells through Inhibition of Mitochondrial Dysfunction and ROS Production. Bio Med Res Int 2014;383-386.
7
8. Mojarrab M, Mehrabi M, Ahmadi F, Hosseinzadeh L, Protective effects of fractions from Artemisia biennis hydroethanolic extract against doxorubicin- induced oxidative stress and apoptosis in PC12 cells. Iran J Basic Med Sci 2016;19:803-810.
8
9. Mojarrab M, Nasseri S, Hosseinzadeh L, Farahani F, Evaluation of antioxidant and cytoprotective activities of Artemisia ciniformis extracts on PC12 cells. Iran J Basic Med Sci 2016; 19: 430-438.
9
10. Roleira FM, Tavares-da-Silva EJ, Varela CL, Costa SC, Silva T, Garrido J, Borges F, Plant derived and dietary phenolic antioxidants: anticancer properties. Food Chem 2015;183: 235-258.
10
11. Sajjadi SE, Ghannad A, Composition of the Essential Oil of Echinophora cinerea (Boiss.) Hedge et Lamond. J Essen Oil Res 2002;14:114-15.
11
12. GhasemiPirbalout,i A, Gholipou,r Z,Chemical composition, antimicrobial and antioxidant activities of essential oil from Echinophora cinerea harvested at two phenological stages. J Essent Oil Res 2016; 1-11.
12
13. Gokbulut I, Bilenler T, Karabulut, I. Determination of chemical composition, total phenolic, antimicrobial, and antioxidant activities of Echinophora tenuifolia essential oil. Int. J Food Prop2013; 16:1442-1451.
13
14. Sharafati-chaleshtoriR, Rafieian-kopaei M, MortezaeiS, Sharafati-chaleshtori A,Amini E, Antioxidant and antibacterial activity of the extracts of Echinophora platyloba DC. Afr. J Pharm Pharmacol 2012;6 :2692-5.
14
15. Shafee-Zadeh F, Medicinal plants of Lorestan (1st ed.): Lorestan University of Med Sci 2002.
15
16. Shokoohinia, Rashidi M, Hosseinzadeh L, Jelodarian Z. Quercetin-3-O-β-D-glucopyranoside, a dietary flavonoid, protects PC12 cells from H2O2-induced cytotoxicity through inhibition of reactive oxygen species. Food Chem 2015;167:162-7.
16
17. Yoo Y, Hong J, Hur KC, Oh E-S, Chung J. Iron enhances NGF-induced neurite outgrowth in PC12 cells Mol Cells2004;17:340-6.
17
18. Jelodarian Z, Shokoohinia Y, Rashidi M, Ghiasvand N, Hosseinzadeh L, Iranshahi M, New polyacetylenes from Echinophora cinerea (Boiss.) Hedge et Lamond..Nat Prod Res 2017:1-8.
18
19. Mosmann T, "Rapid colorimetric assay for cellular growth and survival: application to proliferation and cytotoxicity assays". J Immunol Meth 1983; 65 : 55–63.
19
20. Mojarrab M, Jamshidi M, Ahmadi F, AlizadehE, Hosseinzadeh L. Extracts of Artemisia ciniformis protect cytotoxicity induced by hydrogen peroxide in H9c2 cardiac muscle cells through the inhibition of reactive oxygen species. Adv Pharm Sci 2013;36:10-16.
20
21. Karlsson M, Kurz T, Brunk B, Nilsson S E, Frennesson C.I, “What does the commonly used DCF test for oxidative stress really show?” Biochem J 2010;428:183–190.
21
22. ChandraG, DianaS, Beattie S. Coupling between electron transfer and proton pumping in respiratory chain complexes II+III of Rat Liver Mitochondria". ChinBio ChemJ 1995;11 :200-206.
22
23. ZhangL, Cheng, X-R Juan-JuanH, Lan S, Guan-Hua D. Neuroprotective effects of hyperoside on sodium azide-induced apoptosis in PC12 cells. Chin J Nat Med 2011;9 :450-455.
23
24. Zeiss CJ, The apoptosis-necrosis continuum: Insights from genetically altered mice. Vet Pathol 2003;40 :481-495.
24
25. Salakou S1, Kardamakis D, TsamandasAC, Zolota V, Apostolakis E, Tzelepi, V, PapathanasopoulosP, Bonikos DS, Papapetropoulos T, Petsas T, Increased Bax/Bcl-2 ratio up-regulates caspase-3 and increases apoptosis in the thymus of patients with myasthenia gravis. In Vivo 2007;21 :123-32.
25
26. Shokoohinia Y, Hosseinzadeh L, Alipour M, Mostafaei A, Mohammadi Motlagh HR. Comparative evaluation of cytotoxic and apoptogenic effects of several coumarins on human cancer cell lines: osthole induces apoptosis in p53-deficient H1299 cells. Adv Pharmacol Sci 2014.
26
27. Hosseinzadeh, L, Behravan J, Mosaffa F, Bahrami G, Bahrami A, Karimi G. Curcumin potentiates doxorubicin-induced apoptosis in H9c2 cardiac muscle cells through generation of reactive oxygen species. Food Chem Toxicol 2011;49 :1102-1109.
27
28. DW Li, SunJY, Wang K, Zhang S, HouYJ, Yang, MF. Attenuation of Cisplatin-Induced Neurotoxicity by Cyanidin, a Natural Inhibitor of ROS-Mediated Apoptosis in PC12. Cells Mol Neur Bio 2015; 35:995-1001.
28
29. Chao X, Zhou J, Chen T, Liu W, Dong, W, Qu Y. Neuroprotective effect of osthole against acute ischemic stroke on middle cerebral ischemia occlusion in rats. Brain Res 2010;1363:206-211.
29
30. Hollman PC, van Trijp JM, Buysman MN, vd Gaag MS, Mengelers MJ, de Vries JH, et al. Relative bioavailability of the antioxidant flavonoid quercetin from various foods in man. FEBS Let 1997; 418:152-156.
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31. Lei X1, Chao H, Zhang Z, LvJ, LiS, Wei H1, Xue R1, Li F1, Li Z Neuroprotective effects of quercetin in a mouse model of brain ischemic/reperfusion injury via anti-apoptotic mechanisms based on the Akt pathway. Mol Med Rep 2015; 12:3688-3696.
31
32. Vuković L, Puhović J, Erhardt J, Oršolić N. Neuroprotective effect of quercetin against hydrogen peroxide-induced oxidative injury in P19 neurons. J Mol Neuro Sci 2012; 47:286-299.
32
33. Chen TJ1, Jeng JY, Lin CW, Wu CY, Chen YC. Quercetin inhibition of ROS-dependent and -independent apoptosis in rat glioma C6 cells. Toxicol2006;223 :113-126.
33
34. He Y, Qu S, Wang J, He X, Lin W, Zhen H. Neuroprotective effects of osthole pretreatment against traumatic brain injury in rats. Brain Res2012;1433:127-136.
34
35. Hai-Jie Ji, Jin-Feng Hu, Yong-Hui Wang, Xiao-Yu Chen, Ran Zhou, Nai-Hong Chen. Osthole improves chronic cerebral hypo-perfusion induced cognitive deficits and neuronal damage in hippocampus. Eur J Pharmacol2010; 636: 96–101.
35
ORIGINAL_ARTICLE
Pharmacological effects of a synthetic quinoline, a hybrid of tomoxiprole and naproxen, against acute pain and inflammation in mice: a behavioral and docking study
Objective(s): In the present study, we investigated the potential anti-nociceptive activity and acute anti-inflammatory effect of a synthetic quinoline compound (2-(4-Methoxyphenyl)benzo[h]quinoline-4-carboxylic acid, QC), possessing structural elements of both naproxen and tomoxiprole drugs. Materials and Methods: The anti-nociceptive activity of QC was evaluated using chemical- and thermal-induced nociception models and its acute anti-inflammatory effect was evaluated by xylene-induced ear edema test in mice. Results: QC displayed a dose dependent effect in both acute anti-nociceptive tests (writhing and hot plate). This compound at dose of 6.562 mg/kg showed a high anti-nociceptive effect near equal to diclofenac 5 mg/kg. It also showed high anti-inflammatory effects (less than 6.562 mg/kg) comparable to those of reference drugs diclofenac (5 mg/kg) and celecoxib (100 mg/kg). Docking study showed that this quinoline derivative could inhibit COX-2 enzyme strongly. Conclusion: QC showed high anti-nociceptive and anti-inflammatory effects comparable to reference drugs and can exert its anti-nociceptive and anti-inflammatory activities through COX-2 inhibition.
https://ijbms.mums.ac.ir/article_8588_8d117a69efc273e816e2d88f7e3bd345.pdf
2017-04-01
446
450
10.22038/ijbms.2017.8588
Anti-inflammation
COX-2
Molecular modeling
Naproxen
NSAIDs
Quinoline
Tomoxiprole
Hossein
Hosseinzadeh
hoseinzadehh@mums.ac.ir
1
Pharmaceutical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Fatemeh
Mazaheri
mazaherifateme@yahoo.com
2
Biotechnology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Razieh
Ghodsi
ghodsir@mums.ac.ir
3
Biotechnology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1. Mukherjee S, Pal M. Quinolines: a new hope against inflammation. Drug Discov Today 2013; 18, 389-398.
1
2. Zarghi A, Ghodsi R, Azizi E, Daraie B, Hedayati M, Dadrass O. Synthesis and biological evaluation of new 4-carboxyl quinoline derivatives as cyclooxygenase-2 inhibitors. Bioorg Med Chem 2009; 17: 5312-5317.
2
3. Ghodsi R, Zarghi A, Daraie B, Hedayati M. Design, synthesis and biological evaluation of new 2,3-diarylquinoline derivatives as selective cyclooxygenase-2 inhibitors. Bioorg Med Chem 2010; 18: 1029-1033.
3
4. Zarghi A, Ghodsi R. Design, synthesis, and biological evaluation of ketoprofen analogs as potent cyclooxygenase-2 inhibitors. Bioorg Med Chem 2010; 18: 5855–5860.
4
5. Hanke T, Merk D, Steinhilber D, Geisslinger G, Schubert-Zsilavecz M. Small molecules with anti-inflammatory properties in clinical development. Pharmacol Ther 2016; 157: 163–187.
5
5. Imai K, Takaoka A. Comparing antibody and small-molecule therapies for cancer. Nat Rev Cancer 2006; 6: 714-727.
6
6. Lin WH, Kuo HH, Ho LH, Tseng ML, Siao AC, Hung ChT, Jeng KCh, Hou ChW. Gardenia jasminoides extracts and gallic acid inhibitlipopolysaccharide‐induced inflammation by suppression of JNK2/1 signaling pathways in BV‐2 cells. Iran J Basic Med Sci 2015; 18:555‐562.
7
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ORIGINAL_ARTICLE
Zinc oxide nanoparticle reduced biofilm formation and antigen 43 expressions in uropathogenic Escherichia coli
Objective(s): This study aimed to investigate the effect of zinc oxide nanoparticles (ZnO-np) on biofilm formation and expression of the flu gene in uropathogenic Escherichia coli (UPEC) strains. Materials and Methods: Minimum inhibitory concentration (MIC) of ZnO-np was determined by agar dilution method. The effect of MIC and sub-MIC concentrations of ZnO-np on biofilm formation were determined by microtiter plate assay. The expression level of the flu gene was assessed by Real-Time PCR assay. Results: MIC and sub-MIC ZnO-np concentrations reduced biofilm formation by 50% and 33.4%, respectively. Sub-MIC ZnO-np concentration significantly reduced the flu gene expression in the UPEC isolates (P<0.0001). Conclusion: The sub-MIC concentration of ZnO-np reduces biofilm formation and flu gene expression in UPEC isolates. It is suggested to use nanoparticles for coating medical devices to prevent bacterial colonization.
https://ijbms.mums.ac.ir/article_8589_156514a99b5b33e11cde95765dcec9f2.pdf
2017-04-01
451
456
10.22038/ijbms.2017.8589
Biofilm
Urinary tract infection
Uropathogenic Escherichia coli
Zinc oxide nanoparticle
Ali
Shakerimoghaddam
1
Department of Microbiology, Faculty of Medical Sciences, Golestan University of Medical Sciences, Gorgan, Iran
AUTHOR
Ezzat
Ghaemi
eghaemi@yahoo.com
2
Department of Microbiology, Faculty of Medical Sciences, Golestan University of Medical Sciences, Gorgan, Iran
AUTHOR
Ailar
Jamalli
jamali@goums.ac.ir
3
Laboratory Sciences Research Center, Golestan University of Medical Sciences, Gorgan, Iran
LEAD_AUTHOR
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