ORIGINAL_ARTICLE
Razi’s Al-Hawi and saffron (Crocus sativus): a review
Traditional knowledge can be used as a source for development of new medicines. In the present study, we compare the data on saffron in Razi's Al-Hawi book with modern scientific studies. A computerized search of published articles was performed using MEDLINE, Scopus as well as native references. The search terms used were saffron, Crocus sativus, crocetin, crocin, safranal, Razi, and Al-Hawi. A variety of properties of saffron including diuretic, analgesic, anti-inflammatory, hepatoprotective, appetite suppressant, hypnotic, antidepressant, and bronchodilator effects were mentioned in Al-Hawi. Modern studies also confirmed most of these characteristics. This review indicates that the pharmacological data on saffron and its constituents are similar to those found in Razi’s Al-Hawi monograph and it can be concluded that ethnobotanical information and ancient sources have precious data about medicinal plants that lead to finding new compounds for treatment of several diseases.
https://ijbms.mums.ac.ir/article_6267_89e47d4abc9910933814bddbdb27b0b1.pdf
2015-12-01
1153
1166
10.22038/ijbms.2015.6267
Al-Hawi
Crocin
Crocus sativus L
Razi
Saffron
Safranal
Traditional Medicine
Hamid
Mollazadeh
mollazadehh901@mums.ac.ir
1
Department of Pharmacology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Seyyed Ahmad
Emami
2
Department of Traditional Pharmacy, Department of Pharmacognosy, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Hossein
Hosseinzadeh
hosseinzadehh @ mums.ac.ir
3
Pharmaceutical Research Center, Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical
Sciences, Mashhad, Iran
LEAD_AUTHOR
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144
ORIGINAL_ARTICLE
In vitro and in vivo evaluation of a novel testosterone transdermal delivery system (TTDS) using palm oil base
Objective (s): Transdermal preparations for testosterone are becoming popular because of their unique advantages such as avoidance of first-pass effect, convenience, improved bioavailability, and reduction of systemic side effects. A novel testosterone transdermal delivery system (TDDS) was developed using a palm oil base called HAMINTM (a commercial product) and tested using in vitro and in vivo skin permeability test methods. Materials and Methods: The physical characteristics of the formulation such as particle size and viscosity were determined by using Franz diffusion cell and Brookfield viscometer, respectively. In vivo skin permeability test was performed on healthy rabbits through the skin. Testosterone in serum was analyzed using the validated Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS) technique. Results: In vitro study showed that the cumulative amount of testosterone diffused was between 40 to 1400 ngcm-² over a period of five hr after application of TDDS through the artificial Strat-M™ membrane. In the in vivo rabbit skin permeability test, the results indicated that testosterone was well absorbed with a mean Cmax and Tmax of 60.94 ngml-1 and 2.29 hr after application of TDDS while no increase was observed in placebo treatment. Particle size analysis ranged from 79.4 nm to 630.0 nm for placebo and 97 to 774.0 nm for TDDS. Conclusion: The formulation was successfully prepared using HAMINTM, which has demonstrated great potential for topical delivery of testosterone.
https://ijbms.mums.ac.ir/article_6268_8eb51cd7b50720cc96f418322d1bc3a3.pdf
2015-12-01
1167
1175
10.22038/ijbms.2015.6268
HAMINTM
Skin permeation
Testosterone
Transdermal delivery-
system
Didi Erwandi Mohamad
Haron
didisucxes@gmail.com
1
Shimadzu-UMMC Center for Xenobiotics Studies (SUCXeS), University of Malaya, 50603 Kuala Lumpur, Malaysia
LEAD_AUTHOR
Zamri
Chik
zamrichik@ummc.edu.my
2
Shimadzu-UMMC Center for Xenobiotics Studies (SUCXeS), University of Malaya, 50603 Kuala Lumpur, Malaysia
AUTHOR
Mohamed Ibrahm
Noordin
3
Department of Pharmacy, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia
AUTHOR
Zahurin
Mohamed
zahurin@ummc.edu.my
4
University of Malaya Bioequivalence and Testing Center (UBAT), Department of Pharmacology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia
AUTHOR
1. Mazur A, Booth A. Testosterone and dominance in men. Behav Brain Sci 1998; 21:353-397.
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2. Nieschlag E. Testosterone treatment comes of age: new options for hypogonadal men. Clin Endocrinol 2006; 65:275–281.
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4. Bhasin S, Cunningham GR, Hayes FJ, Matsumoto AM, Snyder PJ, Swerdloff RS et al. Testosterone therapy in adult men with androgen deficiency syndromes: an endocrine society clinical practice guideline. J Clin Endocrinol Metab 2010; 95:2536–2559.
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5. Katznelson L, Finkelstein J, Schoenfeld D, Rosenthal K, Klibanski A. Increase in bone density and lean body mass during testosterone administration in men with acquired hypogonadism. J Clin Endocrinol Metab 1996; 81: 4358–4365.
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6. Behre H, Kliesch S, Leifke R, Link R, Nieschlag E. Long-term effect of testosterone therapy on bone mineral density in hypogonadal men. J Clin Endocrinol Metab 1997; 82:2386-2390.
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7. Wang C, Alexander G, Berman N, Salehian B, Davidson T, McDonald V, et al. Testosterone replacement therapy improves mood in hypogonadal men-a clinical research center study. J Clin Endocrinol Metab 1996; 81:3578-3583.
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8. Handelsman DJ, Conway AJ, Boylan LM. Pharmacokinetics and pharmacodynamics of testosterone pellets In man. J Clin Endocrinol Metab 1990; 71;216-222.
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18. Sakeena M, Muthanna F, Ghassan Z, Kanakal M, Elrashid S, Munavvar A, et al. Formulation and in vitro evaluation of ketoprofen in palm oil esters nanoemulsion for topical delivery. J Oleo Sci 2010; 59:223-228.
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35
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36
ORIGINAL_ARTICLE
The effects of long-term leptin administration on morphometrical changes of mice testicular tissue
Objective(s):Leptin is a novel and interesting hormone for anyone trying to lose weight, but its effects on male gonad structure in longitudinal study is unknown. The present study was designed to explore morphometrical changes of mouse testicular tissue after long-term administration of leptin. Materials and Methods:Thirty healthy mature male mice were randomly assigned to either control (n=15) or treatment (n=15) groups. Leptin was intraperitoneally injected to the treatment group (0.1 µg/100 µl of physiological saline) once a day for 30 consecutive days, and control animals received normal saline with the same volume and route. Five mice from each experimental group were sacrificed at 15, 30 and 60 days after the beginning of treatments. Left testes were removed, weighted and then fixed in 10% buffered formalin, and stained with hematoxylin and eosine for morphometrical assays. Results:Except for sertoli cell nucleus diameter, which was affected from 30th day, evaluation of other morphometrical parameters such as Johnsen’s score, meiotic index, spermatogenesis, epithelial height, seminiferous tubules diameter and spermatogonial nucleus diameter revealed significant decrease from 15th day after leptin administration compare to those of the control group (P<0.05). Thus, meiotic index and spermatogonial cell nucleus diameter were two parameters that were further disturbed on 30th day compare to the day 15 (3.09±0.03 vs. 3.23±0.03, P=0.006 and 5.50±0.09 vs. 6.08±0.14, P=0.007, respectively). Conclusion:Our results showed that long-term administration of leptin could disturb testicular tissue structure and delay spermatogenesis process.
https://ijbms.mums.ac.ir/article_6269_c488a4b5c45f341be0b4793011aaed26.pdf
2015-12-01
1176
1182
10.22038/ijbms.2015.6269
Leptin
Meiotic index
Sertoli cell
Spermatogenesis
Spermatogonia cell
Mohammad-Reza
Esmaili-Nejad
esmaili.mreza@yahoo.com
1
Graduated Student of Veterinary Medicine, Shahid Bahonar University of Kerman, Kerman, Iran
AUTHOR
Homayoon
Babaei
hombabaei@yahoo.com
2
Department of Clinical Sciences, Faculty of Veterinary Medicine, Shahid Bahonar University of Kerman, Kerman, Iran
LEAD_AUTHOR
Reza
Kheirandish
kheirandish@uk.ac.ir
3
Department of Pathobiology, Faculty of Veterinary Medicine, Shahid Bahonar University of Kerman, Kerman, Iran
AUTHOR
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ORIGINAL_ARTICLE
Repeated injections of orexin-A developed behavioral tolerance to its analgesic effects in rats
Objective(s):Reduction of pharmacological effectiveness or tolerance appears following repeated administration of many analgesic drugs. We investigated tolerance to anti-nociceptive effects of orexin-A, an endogenous potent analgesic peptide using the hot-plate test.Materials and Methods:Orexin-A was microinjected ICV (intracerebroventricular) with an interval of 12 hr for 7 continuous days and its anti-nociceptive responses were measured on days 1, 4 and 7 using the hot-plate test following the first day of administration. Orexin-A was used at a dose of 100 pmol to induce analgesic effects. Results:ICV administration of orexin-A produced an effective anti-nociception on the first day of experiment as measured by hot-plate 5, 15, and 30 min after the injection, in comparison with both baselines (hot-plate test one day before the beginning of orexin-A administration and control, saline-administrated group). However, repeated administration of orexin-A on the following days revealed a significant reduction in this analgesic effect during day 4 to day 7. However, to rule out any associative tolerance resulting from learning related to experimental procedures and/or environmental cues, a single injection of orexin-A was administrated to animals of control group (which were receiving saline during 7 days of experiments) and the analgesic effect was observed. Conclusion:These results, for the first time, indicated the appearance of tolerance to anti-nociceptive effects of orexin-A, following repeated administrations of this agent.
https://ijbms.mums.ac.ir/article_6270_fc2693fd0e1ef47a01d28656cca1763b.pdf
2015-12-01
1183
1188
10.22038/ijbms.2015.6270
Anti-nociception
Hot plate
Orexin-A
Tolerance
Elmira
Ghasemi
ghasemi136@yahoo.com
1
Cellular and Molecular Research Center, Sabzevar University of Medical Sciences, Sabzevar, Iran
AUTHOR
Nima
Heidari-Oranjaghi
2
Department of Physiology, Zanjan University of Medical Sciences, Zanjan, Iran
AUTHOR
Hassan
Azhdari-Zarmehri
hasan.azhdari@gmail.com
3
Neuroscience Research Center, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran
LEAD_AUTHOR
Mehdi
Sadegh
msadegh1360@yahoo.com
4
Department of Physiology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran
AUTHOR
1. Mayer DJ, Mao J, Holt J, Price DD. Cellular mechanisms of neuropathic pain, morphine tolerance, and their interactions. Proc Natl Acad Sci U S A 1999; 96:7731-7736.
1
2. Van Vliet BJ, Van Rijswijk AL, Wardeh G, Mulder AH, Schoffelmeer AN. Adaptive changes in the number of Gs- and Gi-proteins underlie adenylyl cyclase sensitization in morphine-treated rat striatal neurons. Eur J Pharmacol 1993; 245:23-29.
2
3. Gintzler AR, Chakrabarti S. Post-opioid receptor adaptations to chronic morphine; altered functionality and associations of signaling molecules. Life Sci 2006; 79:717-722.
3
4. Williams JT, Christie MJ, Manzoni O. Cellular and synaptic adaptations mediating opioid dependence. Physiol Rev 2001; 81:299-343.
4
5. Wong CS, Cherng CH, Luk HN, Ho ST, Tung CS. Effects of NMDA receptor antagonists on inhibition of morphine tolerance in rats: binding at mu-opioid receptors. Eur J Pharmacol 1996; 297:27-33.
5
6. de Lecea L, Kilduff TS, Peyron C, Gao X, Foye PE, Danielson PE, et al. The hypocretins: hypothalamus-specific peptides with neuroexcitatory activity. Proc Natl Acad Sci U S A 1998; 95:322-327.
6
7. Sakurai T. The neural circuit of orexin (hypocretin): maintaining sleep and wakefulness. Nat Rev Neurosci 2007; 8:171-181.
7
8. Sofiabad M, Heidari N, Ghasemi E, Esmaeili MH, Haghdoost-Yazdi H, Erami E, et al. Assesment of orexin receptor 1 in stress attenuated nociceptive behaviours in formalin test. Physiol Pharmacol 2011; 15:395-402.
8
9. Peyron C, Faraco J, Rogers W, Ripley B, Overeem S, Charnay Y, et al. A mutation in a case of early onset narcolepsy and a generalized absence of hypocretin peptides in human narcoleptic brains. Nat Med 2000 ; 6:991-997.
9
10. Trivedi P, Yu H, MacNeil DJ, Van der Ploeg LH, Guan XM. Distribution of orexin receptor mRNA in the rat brain. FEBS Lett 1998; 438:71-75.
10
11. azhdari Zarmehri H, Semnanian S, Fathollahi Y. Comparing the analgesic effects of periaqueductal gray matter injection of orexin A and morphine on formalin- induced nociceptive behaviors. Physiol Pharmacol 2008; 12:188-193.
11
12. Azhdari Zarmehri H, Semnanian S, Fathollahi Y, Erami E, Khakpay R, Azizi H, et al. Intra-periaqueductal gray matter microinjection of orexin-A decreases formalin-induced nociceptive behaviors in adult male rats. J Pain 2011; 12:280-287.
12
13. Bingham S, Davey PT, Babbs AJ, Irving EA, Sammons MJ, Wyles M, et al. Orexin-A, an hypothalamic peptide with analgesic properties. Pain 2001; 92:81-90.
13
14. Ho YC, Lee HJ, Tung LW, Liao YY, Fu SY, Teng SF, et al. Activation of orexin 1 receptors in the periaqueductal gray of male rats leads to antinociception via retrograde endocannabinoid (2-arachidonoylglycerol)-induced disinhibition. J Neurosci 2011; 31:14600-14610.
14
15. Sadeghi S, Reisi Z, Azhdari-Zarmehri H, Haghparast A. Involvement of orexin-1 receptors in the ventral tegmental area and the nucleus accumbens in antinociception induced by lateral hypothalamus stimulation in rats. Pharmacol Biochem Behav 2013; 105:193-198.
15
16. Yamamoto T, Nozaki-Taguchi N, Chiba T. Analgesic effect of intrathecally administered orexin-A in the rat formalin test and in the rat hot plate test. Br J Pharmacol 2002; 137:170-176.
16
17. Yamamoto T, Saito O, Shono K, Aoe T, Chiba T. Anti-mechanical allodynic effect of intrathecal and intracerebroventricular injection of orexin-A in the rat neuropathic pain model. Neurosci Lett 2003 28; 347:183-186.
17
18. Azhdari-Zarmehri H, Esmaeili MH, Sofiabadi M, Haghdoost-Yazdi H. Orexin receptor type-1 antagonist SB-334867 decreases morphine-induced antinociceptive effect in formalin test. Pharmacol Biochem Behav 2013; 112:64-70.
18
19. Heidari-Oranjaghi N, Azhdari-Zarmehri H, Erami E, Haghparast A. Antagonism of orexin-1 receptors attenuates swim- and restraint stress-induced antinociceptive behaviors in formalin test. Pharmacol Biochem Behav 2012; 103:299-307.
19
20.Hervieu GJ, Cluderay JE, Harrison DC, Roberts JC, Leslie RA. Gene expression and protein distribution of the orexin-1 receptor in the rat brain and spinal cord. Neuroscience 2001; 103:777-797.
20
21. Mobarakeh JI, Takahashi K, Sakurada S, Nishino S, Watanabe H, Kato M, et al. Enhanced antinociception by intracerebroventricularly and intrathecally-administered orexin A and B (hypocretin-1 and -2) in mice. Peptides 2005; 26:767-777.
21
22. Trujillo KA. The neurobiology of opiate tolerance, dependence and sensitization: mechanisms of NMDA receptor-dependent synaptic plasticity. Neurotox Res 2002; 4:373-391.
22
23. Pernia-Andrade AJ, Tortorici V, Vanegas H. Induction of opioid tolerance by lysine-acetylsalicylate in rats. Pain 2004; 111:191-200.
23
24. Cheng JK, Chou RC, Hwang LL, Chiou LC. Antiallodynic effects of intrathecal orexins in a rat model of postoperative pain. J Pharmacol Exp Ther 2003; 307:1065-1071.
24
25. Mobarakeh JI, Takahashi K, Sakurada S, Nishino S, Watanabe H, Kato M, et al. Enhanced antinociception by intracerebroventricularly administered orexin A in histamine H1 or H2 receptor gene knockout mice. Pain 2005; 118:254-262.
25
26. Chiou LC, Lee HJ, Ho YC, Chen SP, Liao YY, Ma CH, et al. Orexins/hypocretins: pain regulation and cellular actions. Curr Pharm Des 2010; 16:3089-3100.
26
27. Novak CM, Levine JA. Daily intraparaventricular orexin-A treatment induces weight loss in rats. Obesity 2009; 17:1493-1498.
27
28. Yamanaka A, Sakurai T, Katsumoto T, Yanagisawa M, Goto K. Chronic intracerebroventricular administration of orexin-A to rats increases food intake in daytime, but has no effect on body weight. Brain Res 1999; 849:248-252.
28
29. Kotz CM. Integration of feeding and spontaneous physical activity: role for orexin. Physiol Behav 2006 ; 88:294-301.
29
30. Liu JG, Anand KJ. Protein kinases modulate the cellular adaptations associated with opioid tolerance and dependence. Brain Res Brain Res Rev 2001; 381-319.
30
31. Zhu Y, Miwa Y, Yamanaka A, Yada T, Shibahara M, Abe Y, et al. Orexin receptor type-1 couples exclusively to pertussis toxin-insensitive G-proteins, while orexin receptor type-2 couples to both pertussis toxin-sensitive and -insensitive G-proteins. J Pharmacol Sci 2003; 92:259-266.
31
32. Gorojankina T, Grebert D, Salesse R, Tanfin Z, Caillol M. Study of orexins signal transduction pathways in rat olfactory mucosa and in olfactory sensory neurons-derived cell line Odora: multiple orexin signalling pathways. Regul Pept 2007; 141:73-85.
32
33. Ozcan M, Ayar A, Serhatlioglu I, Alcin E, Sahin Z, Kelestimur H. Orexins activates protein kinase C-mediated Ca(2+) signaling in isolated rat primary sensory neurons. Physiol Res 2010; 59:255-262.
33
ORIGINAL_ARTICLE
Evaluation of the circulating levels of IL-12 and IL-33 in patients with breast cancer: influences of the tumor stages and cytokine gene polymorphisms
Objective(s):IL-12 as an anti-tumor cytokine and IL-33 a novel identified cytokine with both pro- or anti-tumor activities, play important roles in response against tumor cells. Our aim was to evaluate the IL-12 and IL-33 levels and single nucleotide polymorphisms (SNP) in their genes in patients with breast cancer. Materials and Methods:Blood samples were collected from 100 patients with breast cancer, and 100 healthy women were controls. The serum IL-12 and IL-33 levels were measured by ELISA. The SNP rs3212227 (in IL-12 gene) and rs1929992 (in IL-33 gene) were determined using PCR-RFLP. Results:The IL-12 levels similarly expressed in patients and controls. IL-12 levels in patients at stage I were significantly lower than in the healthy group (P<0.05). IL-33 levels and the IL-33/IL-12 ratio were significantly higher in patients than the control group (P<0.001). The IL-33 levels and IL-33/IL-12 ratio in stage IV patients were significantly higher than other stages and controls (PP<0.001, respectively). There were no significant differences in the frequencies of genotypes in rs3212227 and rs1929992 between patients and the control group. No significant differences were observed between subjects with various genotypes at rs3212227 and rs1929992 with respect to related cytokine levels. Conclusion:These results indicate that the diminished IL-12 production may contribute to the tumor establishment. The higher IL-33 levels and IL-33/IL-12 ratio in patients also indicate an imbalance in Th1/Th2 responses that may contribute to tumor development. Thus, correcting the imbalance of Th1/Th2 could be an important strategy for cancer immunotherapy.
https://ijbms.mums.ac.ir/article_6271_2ee6f3de93ae494e9046b7f908a80e08.pdf
2015-12-01
1189
1198
10.22038/ijbms.2015.6271
Breast Cancer
Interleukin-12
Interleukin-33
Single nucleotide -polymorphism
Tumor stages
Abdollah
Jafarzadeh
jafarzadeh14@gmail.com
1
Department of Immunology, Medical School, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
LEAD_AUTHOR
Kayhan
Minaee
keyhanm68@yahoo.com
2
Department of Immunology, Medical School, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Ali-Reza
Farsinejad
3
Department of Laboratory Sciences, Paramedical School, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Maryam
Nemati
nemati_m22@yahoo.com
4
Department of Laboratory Sciences, Paramedical School, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Arezu
Khosravimashizi
akhosravimashizi@yahoo.com
5
Department of Immunology, Medical School, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Hamid
Daneshvar
hamiddaneshvar@hotmail.com
6
Department of Immunology, Medical School, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Mohammad Mehdi
Mohammadi
7
Department of Immunology, Medical School, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Abdolkarim
Sheikhi
sheikhi@queensu.ca
8
Department of Immunology, Medical School, Dezful University of Medical Sciences, Dezful, Iran
AUTHOR
Abbas
Ghaderi
9
Shiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
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7. Standish LJ, Sweet SE, Novack J,Wenner CA, Bridge C, Nelson A, et al. Breast cancer and theimmune system. J Soc Integr Oncol 2008; 6:158–168.
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26. Nakae S, Morita H, Ohno T, Arae K, Matsumoto K, Saito H. Role of interleukin-33 in innate-type immune cells in allergy. Allergol Int 2013; 62:13-20.
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32. Yu JT, Song JH, Wang ND, Wu ZC, Zhang Q, Zhang N, et al. Implication of IL-33 gene polymorphism in Chinese patients with Alzheimer's disease. Neurobiol Aging 2012; 33:e11-14.
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33. Fan D, Ding N, Yang T, Wu S, Liu S, Liu L, et al. Single nucleotide polymorphisms of the interleukin-33 (IL-33) gene are associated with ankylosing spondylitis in Chinese individuals: a case-control pilot study. Scand J Rheumatol 2014; 43:374-379.
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34. Guo L, Zhou X, Guo X, Zhang X, Sun Y. Association of interleukin-33 gene single nucleotide polymorphisms with ischemic stroke in north Chinese population. BMC Med Genet 2013; 14:109.
34
35. Koca SS, Kara M, Deniz F, Ozgen M, Demir CF, Ilhan N, et al. Serum IL-33 level and IL-33 gene polymorphisms in Behcet's disease. Rheumatol Int 2015; 35:471-477.
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36. Mahdi KM, Nassiri MR, Nasiri K. Hereditary genes and SNPs associated with breast cancer. Asian Pac J Cancer Prev 2013; 14:3403-3409.
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37. Murakami S, Okubo K, Tsuji Y, Sakata H, Hamada S, Hirayama R. Serum interleukin-12 levels in patients with gastric cancer. Surg Today 2004; 34:1014-1019.
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38. Miteva L, Stanilov N, Deliysky T, Mintchev N, Stanilova S. Association of polymorphisms in regulatory regions of interleukin-12p40 gene and cytokine serum level with colorectal cancer. Cancer Invest 2009; 27:924-931.
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48
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50
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51
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53
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54
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55
56. Tamandani DM, Shekari M, Suri V. Interleukin-12 gene polymorphism and cervical cancer risk. Am J Clin Oncol 2009; 32:524-528.
56
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57
58. Kaarvatn MH, Vrbanec J, Kulic A, Knezevic J, Petricevic B, Balen S, et al. Single nucleotide polymorphism in the interleukin 12B gene is associated with risk for breast cancer development. Scand J Immunol 2012; 76:329-335.
58
ORIGINAL_ARTICLE
Fluorescence spectra of cardiac myosin and in vivo experiment: studies on daunorubicin-induced cardiotoxicity
Objective(s):The objective of this study was to investigate the interaction of daunorubicin (DNR) and cardiac myosin (CM) and the changes in mice hearts to exhibit DNR-induced cardiotoxicity . Materials and Methods:The interaction between DNR and CM was expressed using fluorescence quenching at pH 4.0-9.0 and 15-37 °C. DNR-induced cardiotoxicity was studied using in vivo experiment. Forty groups mice were used control group in which mice were treated with DNR orally, and three DNR-treated groups in which mice were injected intraperitoneally with DNR at seven bolus doses of 2.0, 4.0, and 6.0 mg/kg body weight, respectively. Heart indices and myocardial enzyme levels were obtained by histopathological and biochemical analysis. Results:The fluorescence quenching mechanism of DNR-CM complex was observed to be a static procedure at 20 °C (pH 7.4), and weakly acidic environment (pH 4.0-6.0) or higher temperature(30-37 °C) promoted the interaction between DNR and CM, causing variations in conformation and normal physiological functions of CM. Thermodynamic studies demonstrated that the binding of DNR to CM was a spontaneous process driven by entropy. It also indicated that hydrophobic interaction and hydrogen bonds may play essential roles in the combination of DNR with CM. In addition, 4.0-6.0 mg/kg DNR-treated mice exhibited obvious histopathological lesion, increase in myocardial enzyme level, and reductions in blood cell count. Conclusion:Our results are valuable for better understanding the particular mode of DNR-CM interaction, and are important to have a deeper insight into the DNR-induced cardiotoxicity.
https://ijbms.mums.ac.ir/article_6272_66fae3914304e4126c22dfc5f0b1942a.pdf
2015-12-01
1199
1208
10.22038/ijbms.2015.6272
Cardiac myosin
Cardiotoxicity
Daunorubicin
Fluorescence quenching
Myocardial enzyme
Yang
Liu
yangl@childrensnational.org
1
Synergy Innovation Center of Biological Peptide Antidiabetics of Hubei Province, Engineering Technology Research Center of Biological Peptide Antidiabetics of Hubei Province, Department of Pharmaceutical Engineering, School of Life Science, Wuchang University of Technology, Wuhan, Hubei Province 430223, China
LEAD_AUTHOR
Chi
Chen
596657894@qq.com
2
Synergy Innovation Center of Biological Peptide Antidiabetics of Hubei Province, Engineering Technology Research Center of Biological Peptide Antidiabetics of Hubei Province, Department of Pharmaceutical Engineering, School of Life Science, Wuchang University of Technology, Wuhan, Hubei Province 430223, China
AUTHOR
Xiaoxiang
Duan
499756486@qq.com
3
Synergy Innovation Center of Biological Peptide Antidiabetics of Hubei Province, Engineering Technology Research Center of Biological Peptide Antidiabetics of Hubei Province, Department of Pharmaceutical Engineering, School of Life Science, Wuchang University of Technology, Wuhan, Hubei Province 430223, China
AUTHOR
Wenting
Ma
1114786562@qq.com
4
Synergy Innovation Center of Biological Peptide Antidiabetics of Hubei Province, Engineering Technology Research Center of Biological Peptide Antidiabetics of Hubei Province, Department of Pharmaceutical Engineering, School of Life Science, Wuchang University of Technology, Wuhan, Hubei Province 430223, China
AUTHOR
Man
Wang
1301330983@qq.com
5
Synergy Innovation Center of Biological Peptide Antidiabetics of Hubei Province, Engineering Technology Research Center of Biological Peptide Antidiabetics of Hubei Province, Department of Pharmaceutical Engineering, School of Life Science, Wuchang University of Technology, Wuhan, Hubei Province 430223, China
AUTHOR
Mengyi
Tu
1129519714@qq.com
6
Synergy Innovation Center of Biological Peptide Antidiabetics of Hubei Province, Engineering Technology Research Center of Biological Peptide Antidiabetics of Hubei Province, Department of Pharmaceutical Engineering, School of Life Science, Wuchang University of Technology, Wuhan, Hubei Province 430223, China
AUTHOR
Ying
Chen
598293075@qq.com
7
Synergy Innovation Center of Biological Peptide Antidiabetics of Hubei Province, Engineering Technology Research Center of Biological Peptide Antidiabetics of Hubei Province, Department of Pharmaceutical Engineering, School of Life Science, Wuchang University of Technology, Wuhan, Hubei Province 430223, China
AUTHOR
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26. Liu Y, Wang D. Administration of chromium (III) and manganese (II) as a potential protective approach against daunorubicin-induced cardiotoxicity: in vitro and in vivo experimental evidence. Biol Trace Elem Res 2013; 156:253-261.
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49
ORIGINAL_ARTICLE
Deregulation of miR-21 and miR-155 and their putative targets after silibinin treatment in T47D breast cancer cells
Objective(s):MicroRNAs (miRNAs) are a class of short RNAs that control the biological processes including cell proliferation, apoptosis and development. Aberrant expression of miRNAs was determined in the different stages of tumor development and metastasis. To study the effect of silibinin on miRNAs expression, we evaluated quantitative expression of miR-21 and miR-155 as two oncomiRs and several potential targets in silibinin-treated T47D cells. Materials and Methods:The rate of proliferation and apoptosis was measured in silibinin-treated and untreated cells. The expression levels of miR-21 and miR-155 were evaluated in T47D cells treated with silibinin (100 µg/ml). Also, their putative targets were predicted in apoptotic pathways using multiple algorithms; as a confirmation, the transcription level of APAF-1, CASP-9 and BID was evaluated. Results:In silibinin-treated cells, death was occurred in a dose and time-dependent manner. miR-21 and miR-155 was downregulated in cells treated with silibinin (100 µg/ml). It is noticeable that the expression of their potential targets including CASP-9 and APAF-1 was increased in silibinin-treated cells after 48 hr. Conclusion:Our findings showed a correlation between the expression of miR-21 and miR-155 and apoptosis in silibinin treated T47D cells. It seems that miRNAs such as miR-21 and miR-155 were regulated by silibinin. Also, increase in the transcript level of APAF-1 and CASP-9 after downregulation of miR-21 and miR-155 might indicate that these genes were targeted by aforementioned miRNAs in T47D cells.
https://ijbms.mums.ac.ir/article_6273_f8c4b58ee76d8ac902300acd34d23fb1.pdf
2015-12-01
1209
1214
10.22038/ijbms.2015.6273
Apoptosis
miR-21
miR-155
Silibinin
T47D cells
Masoud
Maleki Zadeh
malekzademasoud@alumni.ut.ac.ir
1
Department of Cell and Molecular Biology, School of Biology, College of Science, University of Tehran, Tehran, Iran
AUTHOR
Najmeh
Ranji
2
Department of Genetics, College of Science, Rasht Branch, Islamic Azad University, Rasht, Iran
AUTHOR
Nasrin
Motamed
. motamed2@khayam.ut.ac.ir
3
Department of Cell and Molecular Biology, School of Biology, College of Science, University of Tehran, Tehran, Iran
LEAD_AUTHOR
1. Tiwari P, Kumar A, Balakrishnan S, Kushwaha HS, Mishra KP. Silibinin-induced apoptosis in MCF7 and T47D human breast carcinoma cells involves caspase-8 activation and mitochondrial pathway. Cancer Invest 2011; 29:12-20.
1
2. Noh EM, Yi MS, Youn HJ, Lee BK, Lee YR, Han JH, et al. Silibinin enhances ultraviolet B-induced apoptosis in mcf-7 human breast cancer cells. J Breast Cancer 2011; 14:8-13.
2
3. Lee SO, Jeong YJ, Im HG, Kim CH, Chang YC, Lee IS. Silibinin suppresses PMA-induced MMP-9 expression by blocking the AP-1 activation via MAPK signaling pathways in MCF-7 human breast carcinoma cells. Biochem Biophys Res Commun 2007; 354:165-171.
3
4. Nasiri M, Zarghami N, Koshki KN, Mollazadeh M, Moghaddam MP, Yamchi MR, et al. Curcumin and silibinin inhibit telomerase expression in T47D human breast cancer cells. Asian Pac J Cancer Prev 2013; 14:3449-3453.
4
5. Hsieh YS, Chu SC, Yang SF, Chen PN, Liu YC, Lu KH. Silibinin suppresses human osteosarcoma MG-63 cell invasion by inhibiting the ERK-dependent c-Jun/AP-1 induction of MMP-2. Carcinogenesis 2007; 28:977-987.
5
6. Ranji N, Sadeghizadeh M, Shokrgozar MA, Bakhshandeh B, Karimipour M, Amanzadeh A, et al. MiR-17-92 cluster: an apoptosis inducer or proliferation enhancer. Mol Cell Biochem 2013; 380:229-238.
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7. Calin GA, Croce CM. MicroRNA signatures in human cancers. Nat Rev Cancer 2006; 6:857-866.
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8. Tili E, Michaille JJ, Calin GA. Expression and function of micro-RNAs in immune cells during normal or disease state. Int J Med Sci 2008; 5:73-79.
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11
12. Shimizu S, Takehara T, Hikita H, Kodama T, Miyagi T, Hosui A, et al. The let-7 family of microRNAs inhibits Bcl-xL expression and potentiates sorafenib-induced apoptosis in human hepatocellular carcinoma. J Hepatol 2010; 52:698-704.
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13. Yang M, Li Y, Padgett RW. MicroRNAs: Small regulators with a big impact. Cytokine Growth Factor Rev 2005; 16:387-393.
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14. Wang Z, Li Y, Kong D, Ahmad A, Banerjee S, Sarkar FH. Cross-talk between miRNA and Notch signaling pathways in tumor development and progression. Cancer Lett 2010; 292:141-148.
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15. Lal A, Navarro F, Maher CA, Maliszewski LE, Yan N, O'Day E, et al. miR-24 Inhibits cell proliferation by targeting E2F2, MYC, and other cell-cycle genes via binding to "seedless" 3'UTR microRNA recognition elements. Mol Cell 2009; 35:610-625.
15
16. Cho WC. OncomiRs: the discovery and progress of microRNAs in cancers. Mol Cancer 2007; 6:60.
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17. Johnson CD, Esquela-Kerscher A, Stefani G, Byrom M, Kelnar K, Ovcharenko D, et al. The let-7 microRNA represses cell proliferation pathways in human cells. Cancer Res 2007; 67:7713-7722.
17
18. Sarkar FH, Li Y, Wang Z, Kong D, Ali S. Implication of microRNAs in drug resistance for designing novel cancer therapy. Drug Resist Updat 2010; 13:57-66.
18
19. Yang H, Kong W, He L, Zhao JJ, O'Donnell JD, Wang J, et al. MicroRNA expression profiling in human ovarian cancer: miR-214 induces cell survival and cisplatin resistance by targeting PTEN. Cancer Res 2008; 68:425-433.
19
20. Chen YH, Chen CL, Liang CM, Liang JB, Tai MC, Chang YH, et al. Silibinin inhibits ICAM-1 expression via regulation of N-linked and O-linked glycosylation in ARPE-19 cells. Biomed Res Int 2014; 2014:701395.
20
21. Kil WH, Kim SM, Lee JE, Park KS, Nam SJ. Anticancer effect of silibinin on the xenograft model using MDA-MB-468 breast cancer cells. Ann Surg Treat Res 2014; 87:167-173.
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22. Ting H, Deep G, Agarwal R. Molecular mechanisms of silibinin-mediated cancer chemoprevention with major emphasis on prostate cancer. AAPS J 2013; 15:707-716.
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23. Wang ZX, Lu BB, Wang H, Cheng ZX, Yin YM. MicroRNA-21 modulates chemosensitivity of breast cancer cells to doxorubicin by targeting PTEN. Arch Med Res 2011; 42:281-290.
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24. Babashah S, Sadeghizadeh M, Hajifathali A, Tavirani MR, Zomorod MS, Ghadiani M, et al. Targeting of the signal transducer Smo links microRNA-326 to the oncogenic Hedgehog pathway in CD34+ CML stem/progenitor cells. Int J Cancer 2013; 133:579-589.
24
25. Yan LX, Huang XF, Shao Q, Huang MY, Deng L, Wu QL, et al. MicroRNA miR-21 overexpression in human breast cancer is associated with advanced clinical stage, lymph node metastasis and patient poor prognosis. RNA 2008; 14:2348-2360.
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26. Iorio MV, Ferracin M, Liu CG, Veronese A, Spizzo R, Sabbioni S, et al. MicroRNA gene expression deregulation in human breast cancer. Cancer Res 2005; 65:7065-7070.
26
27. Jiang S, Zhang LF, Zhang HW, Hu S, Lu MH, Liang S, et al. A novel miR-155/miR-143 cascade controls glycolysis by regulating hexokinase 2 in breast cancer cells. EMBO J 2012; 31:1985-1998.
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28. Gan R, Yang Y, Yang X, Zhao L, Lu J, Meng QH. Downregulation of miR-221/222 enhances sensitivity of breast cancer cells to tamoxifen through upregulation of TIMP3. Cancer Gene Ther 2014; 21:290-296.
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38
39. Kamarajan P, Sun NK, Sun CL, Chao CC. Apaf-1 overexpression partially overcomes apoptotic resistance in a cisplatin-selected HeLa cell line. FEBS Lett 2001; 505:206-212.
39
ORIGINAL_ARTICLE
SCN1A and SCN1B gene polymorphisms and their association with plasma concentrations of carbamazepine and carbamazepine 10, 11 epoxide in Iranian epileptic patients
Objective (s): From a genetic point of view, epilepsy is a polygenic multifactorial syndrome. The SCN1A and B genes belong to a family of genes that provide instructions for making sodium channels. Understanding the relevance of SCN1A and SCN1B gene polymorphisms to plasma concentration of carbamazepine (CBZ) and its active metabolite carbamazepine 10, 11 epoxide (CBZE), may shed more light on inter-individual variations in response to CBZ. Materials and Methods: In this cross-sectional study, genotype distribution and allele frequency of six non-synonymous exonic single nucleotide polymorphisms (SNPs) of the SCN1A and B genes were selected and determined using PCR-RFLP in 70 epileptic patients treated with CBZ for at least 6 months. The patients had no hepatic or renal diseases and received no medications known to have a major interaction with CBZ. Serum concentrations of CBZ and CBZE were measured using High-Performance Liquid Chromatography (HPLC). Results: The AA, AG and GG alleles of SCN1A were found in 23, 37 and 10 patients, respectively. There were no statistically significant differences in the mean (± standard deviation) of plasma concentrations of CBZ (P=0.8) and CBZE (P=0.1) among these 3 groups. Likewise, there was no statistically significant relationship between SCN1A polymorphisms and CBZ concentration/dose ratio (P=0.7). A significant association was found between CBZ plasma level and CBZ concentration/dose with CBZ daily dose. All patients had the same genotype of SCN1B gene(CC). and no statistical analysis was performed. Conclusion: No significant association between SCN1A gene polymorphisms and plasma levels of CBZ and CBZE were found.
https://ijbms.mums.ac.ir/article_6274_b603a87fbea14d6c63477279b434b544.pdf
2015-12-01
1215
1220
10.22038/ijbms.2015.6274
Carbamazepine Carbamazepine 10-11-
epoxide
Epilepsy
SCN1A
SCN1B
SNP
Soha
Namazi
namazisoha@yahoo.com
1
Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Negar
Azarpira
negarazarpira@yahoo.com ...
2
Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Katayoon
Javidnia
3
Department of Medicinal Chemistry, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Mehrdad
Emami
4
Transgenic Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Rahimeh
Rahjoo
5
Department of Pharmacotherapy, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Razieh
Berahmand
mehrdade2798@yahoo.com
6
Department of Pharmacotherapy, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Afshin
Borhani-Haghighi
neuro.ab@gmail.com
7
Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
LEAD_AUTHOR
1. Ghaem H, Borhani-Haghighi A. Validity and reliability of the Persian epilepsy quality of life questionnaire. Neurosciences (Riyadh) 2010; 15:249-253.
1
2. Asadi-Pooya AA, Emami M, Ashjazadeh N, Nikseresht A, Shariat A, Petramfar P, et al. Reasons for uncontrolled seizures in adults; the impact of pseudointractability. Seizure 2013; 22:271-274.
2
3. Lakhan R, Kumari R, Misra UK, Kalita J, Pradhan S, Mittal B. Differential role of sodium channels SCN1A and SCN2A gene polymorphisms with epilepsy and multiple drug resistance in the north Indian population. Br J Clin Pharmacol 2009; 68:214-220.
3
4. Jang S, Kim M, Nam T, Kim J, Choi S, Lee S, et al. Polymorphisms in the voltage-gated sodium channel genes and antiepileptic efficacy of carbamazepine. J Korean Neurol Assoc. 2009; 27:147-153.
4
5. Yu FH, Catterall WA. Overview of the voltage-gated sodium channel family. Genome Biol 2003; 4:207.
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6.Thompson CH, Kahlig KM, George AL Jr. SCN1A splice variants exhibit divergent sensitivity to commonly used antiepileptic drugs. Epilepsia 2011; 52:1000-1009.
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8. Toldo I, Bruson A, Casarin A, Salviati L, Boniver C, Sartori S, et al. Polymorphisms of the SCN1A gene in children and adolescents with primary headache and idiopathic or cryptogenic epilepsy: is there a linkage? J Headache Pain 2011; 12:435-441.
8
9. Zhou B, Zhou Q, Yin J, Li G, Xu X, Qu J, et al. Comprehensive analysis of the association of SCN1A gene polymorphisms with the retention rate of carbamazepine following monotherapy for new-onset focal seizures in the Chinese Han population. Clin Exp Pharmacol Physiol 2012; 39:379-384.
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22. Bagshaw SM, Mortis G, Doig CJ, Godinez-Luna T, Fick GH, Laupland KB. One-year mortality in critically ill patients by severity of kidney dysfunction: A population-based assessment. Am J Kidney Dis 2006; 48:402-409.
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23. Fong SY, Gao Q, Zuo Z. Interaction of carbamazepine with herbs, dietary supplements, and food: A Systematic Review. Evid Based Complement Alternat Med 2013; 2013:898261.
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25. Uijla SG, Uiterwaalb CSMP, Aldenkampc AP, Carpayd JA, Doelmane JC, Keizerf K, et al. A cross-sectional study of subjective complaints in patients with epilepsy who seem to be well-controlled with anti-epileptic drugs. Seizure 2006; 15:242–248.
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26. Chou IC PC, Tsai FJ. The lack of assossiation between febrile convulsions and polymorphisms in SCN1A. Epilepsy Res 2003; 54:53-57.
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29. Tate SK, Depondt C, Sisodiya SM, Cavalleri GL, Schorge S, Soranzo N, et al. Genetic predictors of the maximum doses patients receive during clinical use of the anti-epileptic drugs carbamazepine and phenytoin. Proc Natl Acad Sci USA 2005; 102:5507-5512.
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30. Hung CC, Chang WL, Ho JL, Tai JJ, Hsieh TJ, Huang HC, et al. Association of polymorphisms in EPHX1, UGT2B7, ABCB1, ABCC2, SCN1A and SCN2A genes with carbamazepine therapy optimization. Pharmacogenomics 2012; 13:159-169.
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31.Zimprich F, Stogmann E, Bonelli S, Baumgartner C, Mueller JC, Meitinger T, et al. A functional polymorphism in the SCN1A gene is not associated with carbamazepine dosages in Austrian patients with epilepsy. Epilepsia 2008; 49:1108-1109.
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32. Haerian BS, Baum L, Kwan P, Tan HJ, Raymond AA, Mohamed Z. SCN1A, SCN2A and SCN3A gene polymorphisms and responsiveness to antiepileptic drugs: a multicenter cohort study and meta-analysis. Pharmacogenomics 2013; 14:1153-1166.
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35
ORIGINAL_ARTICLE
Mesenchymal stem cells can survive on the extracellular matrix-derived decellularized bovine articular cartilage scaffold
Objective (s): The scarcity of articular cartilage defect to repair due to absence of blood vessels and tissue engineering is one of the promising approaches for cartilage regeneration. The objective of this study was to prepare an extracellular matrix derived decellularized bovine articular cartilage scaffold and investigate its interactions with seeded rat bone marrow mesenchymal stem cells (BM-MSCs). Materials and Methods: Bovine articular cartilage that was cut into pieces with 2 mm thickness, were decellularized by combination of physical and chemical methods including snap freeze-thaw and treatment with sodium dodecyl sulfate (SDS). The scaffolds were then seeded with 1, 1’-dioctadecyl-3, 3, 3’, 3’-tetramethylindocarbocyanine perchlorate (DiI) labeled BM-MSCs and cultured for up to two weeks. Results: Histological studies of decellularized bovine articular cartilage showed that using 5 cycles of snap freeze-thaw in liquid nitrogen and treatment with 2.5% SDS for 4 hr led to the best decellularization, while preserving the articular cartilage structure. Adherence and penetration of seeded BM-MSCs on to the scaffold were displayed by histological and florescence examinations and also confirmed by electron microscopy. Conclusion: ECM-derived decellularized articular cartilage scaffold provides a suitable environment to support adhesion and maintenance of cultured BM-MSCs and could be applied to investigate cellular behaviors in this system and may also be useful for studies of cartilage tissue engineering.
https://ijbms.mums.ac.ir/article_6275_824ff9ca7e4909cae9e4a36017983cbd.pdf
2015-12-01
1221
1227
10.22038/ijbms.2015.6275
Articular cartilage
Decellularization Extracellular matrix
Tissue engineering
Amin
Tavassoli
tavassoli.am@gmail.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
Malihe
Akbarzade Niaki
m_niaky@yahoo.com
3
Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran
AUTHOR
Nasser
Mahdavi-Shahri
mahdavin@um.ac.ir
4
Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran
LEAD_AUTHOR
Fahimeh
Shahabipour
shahabipourfahimeh5@gmail.com
5
Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran
AUTHOR
1. Langer R, Vacanti JP. Tissue engineering. Science. 1993;260:920-926.
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27. Ghasroldasht MM, Irfan-Maqsood M, Matin MM, Bidkhori HR, Naderi-Meshkin H, Moradi A, et al. Mesenchymal stem cell based therapy for osteo-diseases. Cell Biol Int. 2014;38:1081-1085.
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40
ORIGINAL_ARTICLE
Case-control study on peroxisome proliferator-activated receptor gamma polymorphism and interaction with HDL on essential hypertension in Chinese Han
Objective(s): To investigate the association of single nucleotide polymorphisms (SNPs) in the peroxisome proliferator-activated receptors gamma (PPARG) with essential hypertension (EH) and additional role of gene– high-density lipoprotein cholesterol (HDL) interaction. Materials and Methods:A total of 1640 patients with EH (806 males, 834 females), with a mean age of 52.5±12.6 years, were selected, including 816 EH patients and 824 controls, who were enrolled from the community. Three SNPs were selected for genotyping in the case–control study: rs10865710, rs709158, rs1805192. Logistic regression model was used to examine the interaction between SNP and HDL on EH, odds ratio (OR) and 95% confidence interval (95% CI) were also calculated. Results: All genotypes were distributed according to Hardy–Weinberg equilibrium in controls. Logistic regression analysis showed an association between genotypes of variants in rs1805192 and decreased EH risk, EH risk was significantly lower in carriers of Ala allele of the rs1805192 polymorphism than those with Pro/Pro (Pro/Ala+ Ala/Ala versus Pro/Pro, adjusted OR (95% CI) =0.65 (0.53–0.83), after covariate adjustment. In addition, the Ala allele of the rs1805192 polymorphism was also associated with diastolic blood pressure (DBP), but not systolic blood pressure (SBP), we also found, by interaction analysis, combined effect of rs1805192 and HDL on EH risk after covariate adjustment. Conclusion: Our results support an important association between rs1805192 minor allele (Ala allele) of PPARG and lower EH risk, the interaction analysis showed a combined effect of Ala- HDL on lower EH risk.
https://ijbms.mums.ac.ir/article_6276_1392be65ed7a9922f06541140155c07d.pdf
2015-12-01
1228
1232
10.22038/ijbms.2015.6276
Essential hypertension
HDL
interaction
PPAR-γ
Single nucleotide poly-
morphisms
Gang
Wang
wanggangcto@163.com
1
Department of Cardiac Surgery, The affiliated Hospital of Qingdao University, Qingdao 266003, China
AUTHOR
Ping
Xu
xupingxi33@163.com
2
Department of Cardiac Surgery, The affiliated Hospital of Qingdao University, Qingdao 266003, China
LEAD_AUTHOR
Wei
Feng
fengwei.sky@163.com
3
Department of Cardiac Surgery, Beijing Fuwai Hospital, Beijing 100037, China
AUTHOR
Xianyan
Jiang
4
Department of Cardiac Surgery, Qingdao Fuwai Hospital, Qingdao 266034, China
AUTHOR
Tao
Zhang
zht13946447995@126.com
5
Department of Cardiac Surgery, Qingdao Fuwai Hospital, Qingdao 266034, China
AUTHOR
Jian
Li
lijian541226@163.com
6
Department of Cardiac Surgery, Qingdao Fuwai Hospital, Qingdao 266034, China
AUTHOR
1. Yagil Y, Yagil C. The search for the genetic basis of hypertension. Curr Opin Nephrol Hypertens 2005; 14:141–147.
1
2. Halperin RO, Sesso HD, Ma J, Buring JE, Stampfer MJ, Gaziano JM. Dyslipidemia and the risk of incident hypertension in men. Hypertension 2006; 47:45-50.
2
3. Guo ZR, Hu XS, Wu M, Zhou MH, Zhou ZY. A prospective study on the association between dyslipidemia and hypertension. Zhonghua Liu Xing Bing Xue Za Zhi 2009; 30:554-558.
3
4. Harada K, Kariya T, Tanaka A, Toba A, Imai Y, Aoyama R, et al. HDL-cholesterol determines nocturnal blood pressure decline in the elderly with treated hypertension. Circulation 2011; 124:A15401.
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5. Gordon DJ, Probstfield JL, Garrison RJ, Neaton JD, Castelli WP, Knoke JD, et al. High-density lipoprotein cholesterol and cardiovascular disease: four prospective American studies. Circulation 1989; 79:8–15.
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6. Hottenga JJ, Boomsma DI, Kupper N, Posthuma D, Snieder H, Willemsen G, et al. Heritability and stability of resting blood pressure. Twin Res Hum Genet 2005; 8:499–508
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7. Tsai YS, Kim HJ, Takahashi N, Kim HS, Hagaman JR, Kim JK, et al. Hypertension and abnormal fat distribution but not insulin resistance in mice with P465L PPAR gamma. J Clin Invest 2004; 114:240–249.
7
8. Gouni-Berthold I, Giannakidou E, Muller-Wieland D, Faust M, Kotzka J, Berthold HK, et al. Peroxisorne proliferator-activated receptor gamma 2 Pro12Ala and endothelial nitric oxide synthase-4a/b gene polymorphisms are not associated with hypertension in diabetes mellitus type 2. J Hypertens 2005; 23: 301–308.
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9. Ostgren CJ, Lindblad U, Melander O, Melander A, Groop L, Rastam L. Peroxisome proliferator activated receptor-gamma Pro12Ala polymorphism and the association with blood pressure in type 2 diabetes: Skaraborg Hypertension and Diabetes Project. J Hypertens 2003; 21: 1657–1662.
9
10. Stefanski A, Majkowska L, Ciechanowicz A, Frankow M, Safranow K, Parczewski M, et al. Association between the Pro12Ala variant of the peroxisome proliferator- activated receptor gamma 2 gene and increased 24-h diastolic blood pressure in obese patients with type II diabetes. J Hum Hypertens 2006; 20:684–692.
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11. World Health Organization. International Society of Hypertension guidelines for the management of hypertension. GuidelinesSubcommittee. J Hypertens 1999; 17:151–183.
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12. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA 2001; 285:2486–2497.
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13. Hardy GH. Mendelian proportions in a mixed population. Science 1908;18:49–5014.
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14. Weinberg W. On the demonstration of heredity in man. In: Boyer SH. editor. Papers on human genetics.1963. Prentice-Hall. Englewood Cliffs NJ; 1908.
14
15. Yen CJ, Beamer BA, Negri C, Silver K, Brown KA, Yarnall DP, et al. Molecular scanning of the human peroxisome proliferator-activated receptor gamma (hPPAR gamma) gene in diabetic Caucasians: identification of a Pro12Ala PPAR gamma 2 missense mutation. Biochem Biophys Res Commun 1997; 241: 270–274.
15
16. Lu Z, Dong B, Mo X, Chen T, Wu H, Zhang Y, et al. Pro12Ala polymorphism in PPAR c 2 associated with essential hypertension in Chinese nonagenarians/-centenarians. Exp Gerontol 2008; 43:1108–1113.
16
17. Gu SJ, Guo ZR, Wu M, Ding Y, Luo WS. Association of peroxisome proliferator-activated receptor g polymorphisms and haplotypes with essential hypertension. Genet Test Mol Biomarkers 2013; 17:1-6.
17
18. Wang Y, Liu C. Quantitative evaluation of common polymorphism (rs1801282) in the PPARg2 gene and hypertension susceptibility. Gene 2012; 502:159–162.
18
19. Oda E, Kawai R. High-density lipoprotein cholesterol is positively associated with hypertension in apparently healthy Japanese men and women. Br J Biomed Sci 2011; 68:29-33.
19
20. Sugawara A, Uruno A, Kudo M, Matsuda K, Yang CW, Ito S. Effects of PPAR-γ on hypertension, atherosclerosis, and chronic kidney disease. Endocr J 2010; 57:847-852.
20
21. Benkirane K, Viel EC, Amiri F, Schiffrin EL. Peroxisome proliferator-activated receptor gamma regulates angiotensin II-stimulated phosphatidyl-inositol 3-kinase and mitogen-activated protein kinase in blood vessels in vivo. Hypertension 2006; 47:102-108.
21
22. Ji Y, Liu J, Wang Z, Liu N, Gou W. PPAR gamma agonist, rosiglitazone, regulates angiotensin II-induced vascular inflammation through the TLR4-dependent signaling pathway. Lab Invest 2009; 89: 887-902.
22
23. Wu L, Wang R, De Champlain J, Wilson TW. Beneficial and deleterious effects of rosiglitazone on hypertension development in spontaneously hypertensive rats. Am J Hypertens 2004; 17:749-756.
23
ORIGINAL_ARTICLE
Effects of cardiopulmonary bypass on lung nuclear factor-kappa B activity, cytokine release, and pulmonary function in dogs
Objective(s): To study the effect of cardiopulmonary bypass (CPB) on nuclear factor-kappa B (NF-кB) and cytokine expression and pulmonary function in dogs. Materials and Methods: Twelve male mongrel dogs were divided into a methylprednisolone group (group M) and a control group (group C). All animals underwent aortic and right atrial catheterization under general anesthesia. Changes in pulmonary function and hemodynamics were monitored and the injured site was histologically evaluated. Results: The activity of NF-кB and myeloperoxidase (MPO), levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-8, and the wet/dry (W/D) weight ratio were significantly higher after CPB than before CPB in both groups (P<0.01), with the lower values in group M than in group C, at different time points (P<0.01). Histological evaluation revealed neutrophilic infiltration and thickening of the alveolar interstitium in both groups; however, the degree of pathological changes was significantly lower in group M than in group C. The alveolar–arterial O2 tension difference (PA-aDO2) was significantly higher after CPB than before CBP (P<0.01), and lower in group M than in group C (P<0.01). The pulmonary compliance after removal of the aortic clamp obviously decreased in group C (P<0.05), with no significant change in group M. Conclusion: CPB can significantly enhance the activation of NF-кB in lung tissues and increase the expression of inflammatory cytokines, thus inducing lung injury. Methylprednisolone can inhibit the NF-кB activation, thus inhibiting the release of cytokines and protecting the lung function.
https://ijbms.mums.ac.ir/article_6277_be937f4393edfd92973d2e6b2f78555c.pdf
2015-12-01
1233
1239
10.22038/ijbms.2015.6277
Acute lung injury
Cardiopulmonary bypass Cytokines
Methyl-prednisolone
NF-кB
Gaisheng
Yang
gaishengyang@163.com
1
Department of Anesthesiology, Airforce General Hospital, Beijing 100142, China
LEAD_AUTHOR
Xiaodong
Xue
xuexdbj@163.com
2
Department of Anesthesiology, Airforce General Hospital, Beijing 100142, China
AUTHOR
Yanying
Chen
chenyy6@yeah.net
3
Department of Anesthesiology, Airforce General Hospital, Beijing 100142, China
AUTHOR
Zhihong
Song
dilidaerxi@yeah.net
4
Department of Anesthesiology, Airforce General Hospital, Beijing 100142, China
AUTHOR
Zhen
Jiang
15020708763@163.com
5
Department of Anesthesiology, the Affiliated Zhongshan Hospital of Fudan University, Shanghai 200032, China
AUTHOR
Kejian
Hu
kejianhucn@yeah.net
6
Department of Extracorporeal Circulation, the Affiliated Zhongshan Hospital of Fudan University, Shanghai 200032, China
AUTHOR
1.Apostolakis E, Filos KS, Koletsis E, Dougenis D. Lung dysfunction following cardiopulmonary bypass. J Card Surg 2010; 25:47-55.
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2.Onorati F, Rubino AS, Nucera S, Foti D, Sica V, Santini F, et al. Off-pump coronary artery bypass surgery versus standard linear or pulsatile cardiopulmonary bypass: endothelial activation and inflammatory response. Eur J Cardiothorac Surg 2010; 37:897-904.
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3.Ng CS, Hui CW, Wan S, Wan IY, Ho AM, Lau KM, et al. Lung ischaemia-reperfusion induced gene expression. Eur J Cardiothorac Surg 2010; 37:1411-1420.
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4.Larsen BM, Goonewardene LA, Joffe AR, Van Aerde JE, Field CJ, Olstad DL, et al. Pre-treatment with an intravenous lipid emulsion containing fish oil (eicosapentaenoic and docosahexaenoic acid) decreases inflammatory markers after open-heart surgery in infants: a randomized, controlled trial. Clin Nutr 2012; 31:322-329.
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5.Pearl JM, Schwartz SM, Nelson DP, Wagner CJ, Lyons JM, Bauer SM, et al. Preoperative glucocorticoids decrease pulmonary hypertension in piglets after cardiopulmonary bypass and circulatory arrest. Ann Thorac Surg 2004; 77:994-1000.
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6.Ng CS, Arifi AA, Wan S, Ho AM, Wan IY, Wong EM, et al. Ventilation during cardiopulmonary bypass: impact on cytokine response and cardiopulmonary function. Ann Thorac Surg 2008; 85:154-162.
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7.Goebel U, Siepe M, Mecklenburg A, Doenst T, Beyersdorf F, Loop T, et al. Reduced pulmonary inflammatory response during cardiopulmonary bypass: effects of combined pulmonary perfusion and carbon monoxide inhalation. Eur J Cardiothorac Surg 2008; 34:1165-1172.
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8.Onorati F, Santarpino G, Tangredi G, Palmieri G, Rubino AS, Foti D, et al. Intra-aortic balloon pump induced pulsatile perfusion reduces endothelial activation and inflammatory response following cardiopulmonary bypass. Eur J Cardiothorac Surg 2009; 35:1012-1019.
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9.Onorati F, Santini F, Mariscalco G, Bertolini P, Sala A, Faggian G, et al. Leukocyte filtration ameliorates the inflammatory response in patients with mild to moderate lung dysfunction. Ann Thorac Surg 2011; 92:111-121.
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10.Mangoush O, Purkayastha S, Haj-Yahia S, Kinross J, Hayward M, Bartolozzi F, et al. Heparin-bonded circuits versus nonheparin-bonded circuits: an evaluation of their effect on clinical outcomes. Eur J Cardiothorac Surg 2007; 31:1058-1069.
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12.Al-Ruzzeh S, Ambler G, Asimakopoulos G, Omar RZ, Hasan R, Fabri B, et al. Off-pump coronary artery bypass (OPCAB) surgery reduces risk-stratified morbidity and mortality: a United Kingdom Multi-Center Comparative Analysis of Early Clinical Outcome. Circulation 2003; 108:II1-8.
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13.Liu SF, Malik AB. NF-kappa B activation as a pathological mechanism of septic shock and inflammation. Am J Physiol Lung Cell Mol Physiol 2006; 290:L622-645.
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19.Ovrum E, Mollnes TE, Fosse E, Holen EA, Tangen G, Abdelnoor M, et al. Complement and granulocyte activation in two different types of heparinized extracorporeal circuits. J Thorac Cardiovasc Surg 1995; 110:1623-1632.
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20.Kirklin JK, Chenoweth DE, Naftel DC, Blackstone EH, Kirklin JW, Bitran DD, et al. Effects of protamine administration after cardiopulmonary bypass on complement, blood elements, and the hemodynamic state. Ann Thorac Surg 1986; 41:193-199.
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21.Shastri KA, Logue GL, Stern MP, Rehman S, Raza S. Complement activation by heparin-protamine complexes during cardiopulmonary bypass: effect of C4A null allele. J Thorac Cardiovasc Surg 1997; 114:482-488.
21
22.Khabar KS, elBarbary MA, Khouqeer F, Devol E, al-Gain S, al-Halees Z. Circulating endotoxin and cytokines after cardiopulmonary bypass: differential correlation with duration of bypass and systemic inflammatory response/multiple organ dysfunction syndromes. Clin Immunol Immunopathol 1997; 85:97-103.
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23.Clark SC. Lung injury after cardiopulmonary bypass. Perfusion 2006; 21:225-228.
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24.Zhou X, Dai Q, Huang X. Neutrophils in acute lung injury. Front Biosci (Landmark Ed) 2012; 17:2278-2283.
24
25.McKay LI, Cidlowski JA. Cross-talk between nuclear factor-kappa B and the steroid hormone receptors: mechanisms of mutual antagonism. Mol Endocrinol 1998; 12:45-56.
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26.Auphan N, DiDonato JA, Rosette C, Helmberg A, Karin M. Immunosuppression by glucocorticoids: inhibition of NF-kappa B activity through induction of I kappa B synthesis. Science 1995; 270:286-290.
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27.McKay LI, Cidlowski JA. CBP (CREB binding protein) integrates NF-kappaB (nuclear factor-kappaB) and glucocorticoid receptor physical interactions and antagonism. Mol Endocrinol 2000; 14:1222-1234.
27
28.De Bosscher K, Vanden Berghe W, Haegeman G. The interplay between the glucocorticoid receptor and nuclear factor-kappaB or activator protein-1: molecular mechanisms for gene repression. Endocr Rev 2003; 24:488-422.
28
29.Lodge AJ, Chai PJ, Daggett CW, Ungerleider RM, Jaggers J. Methylprednisolone reduces the inflammatory response to cardiopulmonary bypass in neonatal piglets: timing of dose is important. J Thorac Cardiovasc Surg 1999; 117:515-522.
29
30.Yuan SM. Postperfusion lung syndrome: physio-pathology and therapeutic options. Rev Bras Cir Cardiovasc 2014; 29:414-425.
30
31.Apostolakis EE, Koletsis EN, Baikoussis NG, Siminelakis SN, Papadopoulos GS. Strategies to prevent intraoperative lung injury during cardiopulmonary bypass. J Cardiothorac Surg 2010; 5:1-9.
31
32.Kiessling AH, Guo FW, Gökdemir Y, Thudt M, Reyher C, Scherer M, et al. The influence of selective pulmonary perfusion on the inflammatory response and clinical outcome of patients with chronic obstructive pulmonary disease undergoing cardiopulmonary bypass. Interact Cardiovasc Thorac Surg 2014; 18:732-739.
32
33.Torina AG, Silveira-Filho LM, Vilarinho KA, Eghtesady P, Oliveira PP, Sposito AC, et al. Use of modified ultrafiltration in adults undergoing coronary artery bypass grafting is associated with inflammatory modulation and less postoperative blood loss: a randomized and controlled study. Thorac Cardiovasc Surg 2012; 144:663-670.
33
34.Curtis N, Vohra HA, Ohri SK. Mini extracorporeal circuit cardiopulmonary bypass system: a review. Perfusion 2010; 25:115-124.
34
35.Tassani P, Richter JA, Barankay A, Braun SL, Haehnel C, et al. Does high-dose methylprednisolone in aprotinin-treated patients attenuate the systemic inflammatory response during coronary artery bypass grafting procedures? J Cardiothorac Vasc Anesth 1999; 13:165-172.
35
36.Chaney MA, Durazo-Arvizu RA, Nikolov MP, Blakeman BP, Bakhos M. Methylprednisolone does not benefit patients undergoing coronary artery bypass grafting and early tracheal extubation. Thorac Cardiovasc Surg 2001; 121:561-569.
36
ORIGINAL_ARTICLE
Screening and identification of SUMP-proteins in sub-acute treatment with diazinon
Objective(s):Small ubiquitin-like modifiers (SUMOs) are a family of ubiquitin-related, proteins that are involved in a wide variety of signaling pathways. SUMOylation, as a vital post translational modification, regulate protein function in manycellular processes. Diazinon (DZN), an organophosphate insecticide, causses oxidative stress and subsequently programmed cell death in different tissues. The aim of this study was to evaluate the role and pattern of SUMO modificationas a defense mechanism against stress oxidative, in the heart tissuesof the DZN treated rats. Materials and Methods: Diazinon (15 mg/kg/day), corn oil (control) were administered via gavageto male Wistar rats for four weeks. SUMO1 antibody was covalently crosslinked to protein A/G agarose. heart tissue lysate were added to agarosebeads,After isolation of target proteins(SUMO1- protein)SDS-PAGE gel electrophoresis was performed. Protein bands were identified using MALDI-TOF/TOF and MASCOT). Fold change of (DZN/Ctrl) separated proteins was evaluated using UVband software (UVITEC, UK). Results:Our result showed that subacute exposure to DZN increased SUMOylationoffour key proteins involved in the metabolic process including; Acyl-CoA dehydrogenase, creatine kinase, glyceraldehyde-3-phosphate dehydrogenase and ATP synthase, in the heart tissue of animals .A probability value of less than 0.05 was considered significant (P<0.05). Conclusion: It seems that protein SUMOylation provides a safeguard mechanism against DZN Toxicity.
https://ijbms.mums.ac.ir/article_6278_a6a1f53ba424d61e89f66bd495e9bf2f.pdf
2015-12-01
1240
1244
10.22038/ijbms.2015.6278
Diazinon
MALDI-TOF/TOF
SUMOlation
SUMO1
Rezvan
Yazdian-Robati
1
Department of Biotechnology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Atena
Pourtaji
pourtajia901@mums.ac.ir
2
Department of Pharmacodynamy and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Marzieh
Rashedinia
3
Department of Toxicology and pharmacology, School of Pharmacy, international branch, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Hossein
Hosseinzadeh
hosseinzadehh @ mums.ac.ir
4
Pharmaceutical Research Center, Department of Pharmacology and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Maryam
Ghorbani
ghorbanim@gmail.com
5
Department of Pharmacology and Toxicology, School of Pharmacy, Baqiyatallah University of Medical Sciences, Tehran, Iran
AUTHOR
BiBi Marjan
Razavi
6
Targeted Drug Delivery Research Center, Department of Pharmacology and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mohammad
Ramezani
m.ramazani@mums.ac.ir
7
Pharmaceutical Research Center, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Khalil
Abnous
abnouskh@mums.ac.ir
8
Pharmaceutical Research Center, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1. Baczyk D, Drewlo S, Kingdom JC. Emerging role of SUMOylation in placental pathology. Placenta. 2013;34:606-612.
1
2. Girdwood DW, Tatham MH, Hay RT. SUMO and transcriptional regulation.Cell Dev Biol. 2004;15:201-210.
2
3.Desterro JMP, Rodriguez MS, Hay RT. SUMO-1 Modification of IκBα Inhibits NF-κB Activation. Molecular Cell. 1998;2:233-239.
3
4. Bawa-Khalfe T, Yeh ET. SUMO Losing Balance: SUMO Proteases Disrupt SUMO Homeostasis to Facilitate Cancer Development and Progression. Genes cancer. 2010;1:748-752.
4
5.Dasso M. Emerging roles of the SUMO pathway in mitosis. Cell Div. 2008;3:5.
5
6.Terashima T, Kawai H, Fujitani M, Maeda K, Yasuda H. SUMO-1 co-localized with mutant atrophin-1 with expanded polyglutamines accelerates intranuclear aggregation and cell death. Neuroreport. 2002;13:2359-2364.
6
7. Pountney DL, Huang Y, Burns RJ, Haan E, Thompson PD, Blumbergs PC, et al. SUMO-1 marks the nuclear inclusions in familial neuronal intranuclear inclusion disease. Exp Neural. 2003;184:436-446.
7
8.McMillan LE, Brown JT, Henley JM, Cimarosti H. Profiles of SUMO and ubiquitin conjugation in an Alzheimer's disease model. Neuroscience letters. 2011;502:201-208.
8
9.Hay RT. SUMO: a history of modification. Mol Cell. 2005;18:1-12.
9
10. Dangoumau A, Veyrat-Durebex C, Blasco H, Praline J, Corcia P, Andres CR, et al. Protein SUMOylation, an emerging pathway in amyotrophic lateral sclerosis. Int J neurosci. 2013;123:366-74.
10
11. Shah MD, Iqbal M. Diazinon-induced oxidative stress and renal dysfunction in rats. Food chem toxical : an international journal published for the British Industrial Biological Research Association. 2010;48:3345-3353.
11
12. Ogutcu A, Uzunhisarcikli M, Kalender S, Durak D, Bayrakdar F, Kalender Y. The effects of organophosphate insecticide diazinon on malondialdehyde levels and myocardial cells in rat heart tissue and protective role of vitamin E. Pesticide Biochemistry and Physiology. 2006;86:93-98.
12
13. Razavi BM, Hosseinzadeh H, Movassaghi AR, Imenshahidi M, Abnous K. Protective effect of crocin on diazinon induced cardiotoxicity in rats in subchronic exposure. Chemico-biological interactions. 2013;203:547-555.
13
14.Handy RD, Abd-El Samei HA, Bayomy MF, Mahran AM, Abdeen AM, El-Elaimy EA. Chronic diazinon exposure: pathologies of spleen, thymus, blood cells, and lymph nodes are modulated by dietary protein or lipid in the mouse. Toxicology. 2002;172:13-34.
14
15. Yavuz T, Delibas N, Yildirim B, Altuntas I, Candır O, Cora A, et al. Vascular wall damage in rats induced by organophosphorus insecticide methidathion. Toxicology Letters. 2005;155:59-64.
15
16. Feligioni M, Nistico R. SUMO: a (oxidative) stressed protein. Neuromolecular Med. 2013;15:707-719.
16
17. Jafari M, Salehi M, Ahmadi S, Asgari A, Abasnezhad M, Hajigholamali M. The role of oxidative stress in diazinon-induced tissues toxicity in Wistar and Norway rats. Toxicol Mech Methods. 2012;22:638-647.
17
18. Yang P, Hu S, Yang F, Guan X-Q, Wang S-Q, Zhu P, et al. Sumoylation modulates oxidative stress relevant to the viability and functionality of pancreatic beta cells. American Journal of Translational Research. 2014:353-360.
18
19. Sirover MA. New insights into an old protein: the functional diversity of mammalian glyceraldehyde-3-phosphate dehydrogenase. Biochim Bio phys Acta. 1999;1432:159-184.
19
20. Hariri AT, Moallem SA, Mahmoudi M, Memar B, Hosseinzadeh H. Sub-acute effects of diazinon on biochemical indices and specific biomarkers in rats: protective effects of crocin and safranal. Food Chemical Toxicol : an international journal published for the British Industrial Biological Research Association. 2010;48:2803-2808.
20
21. Agbor TA, Cheong A, Comerford KM, Scholz CC, Bruning U, Clarke A, et al. Small ubiquitin-related modifier (SUMO)-1 promotes glycolysis in hypoxia. J Biol Chem. 2011;286:4718-4726.
21
22. Kim KI, Baek SH. Small ubiquitin-like modifiers in cellular malignancy and metastasis. Int Rev Cell Mol Biol. 2009;273:265-311.
22
23. Bell RD, Khan M. Cerebrospinal fluid creatine kinase-BB activity: a perspective. Arch Neurol. 1999;56:1327-1328.
23
24. Konorev EA, Hogg N, Kalyanaraman B. Rapid and irreversible inhibition of creatine kinase by peroxynitrite. FEBS lett. 1998;427:171-174.
24
25. Venkataraman P, Krishnamoorthy G, Selvakumar K, Arunakaran J. Oxidative stress alters creatine kinase system in serum and brain regions of polychlorinated biphenyl (Aroclor 1254)-exposed rats: protective role of melatonin. Basic Clin pharmacol toxicol. 2009;105:92-97.
25
26. Schlattner U, Tokarska-Schlattner M, Wallimann T. Mitochondrial creatine kinase in human health and disease. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 2006;1762:164-180.
26
27. Zhang X, Takano T, Liu S. Identification of a mitochondrial ATP synthase small subunit gene (RMtATP6) expressed in response to salts and osmotic stresses in rice (Oryza sativa L.) J Exp Bot. 2006;57:193-200.
27
28. Martinez-Reyes I, Cuezva JM. The H(+)-ATP synthase: a gate to ROS-mediated cell death or cell survival. Biochim Biophys Acta. 2014;1837:1099-1112.
28
29. Johnson ES. Protein modification by SUMO. Annual review of biochemistry. 2004;73:355-382.
29
30. Pandey D, Chen F, Patel A, Wang CY, Dimitropoulou C, Patel VS, et al. SUMO1 negatively regulates reactive oxygen species production from NADPH oxidases. Arterioscler thromb Vasc Biol. 2011;31:1634-1642.
30
ORIGINAL_ARTICLE
Improvement effect of Lycium barbarum polysaccharide on sub-health mice
Objective(s):Sub-health has been described as a chronic condition of unexplained deteriorated physiological function, which falls between health and illness. In the present study, we evaluated the effects of Lycium barbarum polysaccharide (LBP), a polysaccharide fraction purified from Lycium barbarum (L. barbarum) on the sub-health mice. Materials and Methods:The sub-health model mice were built through compound factors. The mice were given intragastric administration of LBP at low dose (50 mg•kg-1) and high dose (100 mg•kg-1), respectively. After LBP treatment for 4 weeks, the antioxidant ability, enhancing immune function and anti-fatigue activity were detected. Results:The results showed that LBP could enhance antioxidant ability in sub-health mice. LBP could effectively improve immunity of sub-health mice and protect the immune organs, such as thymus. In addition, LBP showed anti-fatigue ability in sub-health mice. Conclusion:LBP could improve sub-health state caused from composite factor through three aspects, such as increasing antioxidant ability, promoting T lymphocyte proliferation, inhibiting thymus lymphocyte apoptosis, and alleviating fatigue.
https://ijbms.mums.ac.ir/article_6281_da32b60fb9b6ae600b4ae6528a5ebdbb.pdf
2015-12-01
1245
1252
10.22038/ijbms.2015.6281
Anti-fatigue
Antioxidant
Immunity
Lycium bararum
Polysaccharide
Sub-health
Rui
Zhao
zr601@163.com
1
Department of Pharmaceutical Engineering, College of Life Science & Biotechnology, Heilongjiang August First Land Reclamation University, Daqing High-Tech Industrial Development Zone, 163319, P.R. China
LEAD_AUTHOR
Wenli
Hao
lxy_811@163.com
2
Department of Pharmaceutical Engineering, College of Life Science & Biotechnology, Heilongjiang Bayi Agricultural University, Daqing High-Tech Industrial Development Zone, 163319, P.R. China
AUTHOR
Baoling
Ma
mabaoling528@163.com
3
Department of physical education, Hebei Normal University of Science and Technology, 360 Hebei Street, Qinhuangdao 066004, P.R. China
AUTHOR
Zhibao
Chen
4
Department of Pharmaceutical Engineering, College of Life Science & Biotechnology, Heilongjiang Bayi Agricultural University, Daqing High-Tech Industrial Development Zone, 163319, P.R. China
AUTHOR
1. Dunstan RH, Sparkes DL, Roberts TK, Crompton MJ, Gottfries J, Dascombe BJ. Development of a complex amino acid supplement, Fatigue Reviva™, for oral ingestion: initial evaluations of product concept and impact on symptoms of sub-health in a group of males. Nutr J 2013; 12:115-123.
1
2. Wang W, Russell A, Yan Y, Global Health Epide-miology Reference Group (GHERG). Traditional Chinese medicine and new concepts of predictive, preventive and personalized medicine in diagnosis and treatment of suboptimal health. EPMA J 2014; 5:4-13.
2
3. Huyan T, Li Q, Yang H, Jin ML, Zhang MJ, Ye LJ, et al. Protective effect of polysaccharides on simulated microgravity-induced functional inhibition of human NK cells. Carbohydr Polym 2014;101:819-827.
3
4. Chen JR, Li EQ, Dai CQ, Yu B, Wu XL, Huang CR, et al. The inducible effect of LBP on maturation of dendritic cells and the related immune signaling pathways in hepatocellular carcinoma (HCC). Curr Drug Deliv 2012; 4:414-420.
4
5. Zhao R, Li QW, Li J, Zhang T. Protective effect of Lycium barbarum polysaccharide 4 on kidneys in streptozotocin induced diabetic rats. Can J Physiol Pharmacol 2009;87: 711-719.
5
6. Singh A, Naidu PS, Gupta S, Kulkarni SK. Effect of natural and synthetic antioxidants in a mouse model of chronic fatigue syndrome. J Med Food 2002; 5:211-220.
6
7. Rajeevan MS, Dimulescu I, Murray J, Falkenberg VR, Unger ER. Pathway-focused genetic evaluation of immune and inflammation related genes with chronicfatigue syndrome. Hum Immunol 2015; 15:00180-9.
7
8. Zhao R, Qiu B, Li Q, Zhang T, Zhao H, Chen Z, et al. LBP-4a improves insulin resistance via translocation and activation of GLUT4 in OLETF rats. Food Funct 2014; 5:811-820.
8
9. Wang J, Sun CX, Zheng Y, Pan H, Zhou Y, Fan Y. The effective mechanism of the polysaccharides from Panax ginsengon chronic fatigue syndrome. Arch Pharm Res 2014; 37:530-538.
9
10. Li YP, Huang SH, Jin W. Construction of a sub-health fatigue rat model. Chin J Tissue Engin Res 2011; 7:1225-1228.
10
11. Jiang CM, Chen XL, Lu GF, Chen XY, Wang DY, Hu YL, et al. Comparative study on chicken peripheral lymphocyte and spleen lymphocyte proliferation by Chinese herbal medicinal polysaccharides in vitro. Jiangsu J of Agr Sci 2015; 31:106-111.
11
12. Luo Q, Cai Y, Yan J, Sun M, Corke H. Hypoglycemic and hypolipidemic effects and antioxidant activity of fruit extracts from Lycium barbarum. Life Sci2004; 76:137-149.
12
13. Tian DH. Practical thesaurus of Chinese traditional medicine. People’s Medical Publishing House, Beijing; 2002.p.1348-1354.
13
14. Wang J. Pharmacological action of Lycium barbarum and the analysis of clinical application value. Asia-Pacific Traditional Med2014; 10:50-51.
14
15. Powers SK, Jackson MJ. Exercise-induced oxidative stress: cellular mechanisms and impact on muscle force production. Physiol Rev 2008; 88:1243-1276.
15
16. Ekert PG, Vaux DL. The mitochondrial death squad: hardened killers or innocent bystanders? Curr Opin Cell Biol 2005; 6:626-630.
16
17. Joza N, Susin SA, Daugas E, Stanford WL, Cho SK, Li CYJ. Essential role of the mitochondrial apoptosis-inducing factor in programmed cell death. Nature 2001; 6828: 549-554.
17
18. Susin SA, Daugas E, Ravagnan L, Samejima K, Zamzami N, Loeffler M, et al. Two distinct pathways leading to nuclear apoptosis. J Exp Med 2000; 4:571-580.
18
19. Li J, Jin YJ. Epidemiological surveys of sub-health state and syndrome differentiation of Traditional Chinese Medicine. Chin J Clin Rehabil 2004; 9:1756.
19
20. Castro-Marrero J, Cordero MD, Sáez-Francas N, Jimenez-Gutierrez C, Aguilar-Montilla FJ, Aliste L, et al. Could mitochondrial dysfunction be a differentiating marker between chronic fatigue syndrome and fibromyalgia? Antioxid Redox Signal 2013; 15:1855-60.
20
21. Filler K, Lyon D, Bennett J, McCain N, Elswick R, Lukkahatai N, et al. Association of mitochondrial dysfunction and fatigue: a review of the literature. BBA Clin 2014; 1:12-23.
21
ORIGINAL_ARTICLE
Cholesterol suppresses antimicrobial effect of statins
Objective(s):Isoprenoid biosynthesis is a key metabolic pathway to produce a wide variety of biomolecules such as cholesterol and carotenoids, which target cell membranes. On the other hand, it has been reported that statins known as inhibitors of isoprenoid biosynthesis and cholesterol lowering agents, may have a direct antimicrobial effect on the some bacteria. The exact action of statins in microbial metabolism is not clearly understood. It is possible that statins inhibit synthesis or utilization of some sterol precursor necessary for bacterial membrane integrity. Accordingly, this study was designed in order to examine if statins inhibit the production of a compound, which can be used in the membrane, and whether cholesterol would replace it and rescue bacteria from toxic effects of statins. Materials and Methods: To examine the possibility we assessed antibacterial effect of statins with different classes; lovastatin, simvastatin, and atorvastatin, alone and in combination with cholesterol on two Gram-positive (Staphylococcus aureus and Enterococcus faecalis) and two Gram-negative (Pseudomonas aeruginosa and Escherichia coli) bacteria using gel diffusion assay. Results: Our results showed that all of the statins except for lovastatin had significant antibacterial property in S. aureus, E. coli, and Enter. faecalis. Surprisingly, cholesterol nullified the antimicrobial action of effective statins in statin-sensitive bacteria. Conclusion: It is concluded that statins may deprive bacteria from a metabolite responsible for membrane stability, which is effectively substituted by cholesterol.
https://ijbms.mums.ac.ir/article_6282_9408d113947a4b087da67083a9300383.pdf
2015-12-01
1253
1256
10.22038/ijbms.2015.6282
Bacteria
Hydroxymethylglutaryl coenzyme A
Statin
Sterol
Mohammad Reza
Haeri
haeri@muq.ac.ir
1
Department of Clinical Biochemistry, School of Medicine, Qom University of Medical Sciences, Qom, Iran
LEAD_AUTHOR
Kenneth
White
2
Institute for Health Research and Policy, London Metropolitan University, London, United Kingdom
AUTHOR
Mohammad
Qharebeglou
3
Islamic azad university, Qom branch, Qom-Iran
AUTHOR
Malek Moein
Ansar
4
Department of Clinical Biochemistry, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran
AUTHOR
1. Matsumi R, Atomi H, Driessen AJ, van der Oost J. Isoprenoid biosynthesis in Archaea--biochemical and evolutionary implications. Res Microbiol 2011; 162:39-52.
1
2. Heuston S, Begley M, Gahan CG, Hill C. Isoprenoid biosynthesis in bacterial pathogens. Microbiology 2012; 158:1389-1401.
2
3. Noh DO, Kim SH, Gilliland SE. Incorporation of cholesterol into the cellular membrane of Lactobacillus acidophilus ATCC 43121. J Dairy Sci 1997; 80:3107-3113.
3
4. Dambekodi PC, Gilliland SE. Incorporation of cholesterol into the cellular membrane of Bifidobacterium longum. J Dairy Sci 1998; 81:1818-1824.
4
5. Hildebrandt E. and McGee DJ. Helicobacter pylori lipopolysaccharide modification, Lewis antigen expression, and gastric colonization are cholesterol-dependent. BMC Microbiol 2009; 9:258.
5
6. Li G. Intestinal probiotics: Interactions with bile salts and reduction of cholesterol. Procedia Environ Sci 2012; 12:1180-186.
6
7. McGee DJ, George AE, Trainor EA, Horton KE, Hildebrandt E, Testerman TL. Cholesterol enhances Helicobacter pylori resistance to antibiotics and LL-37. Antimicrob Agents Chemother 2011; 55:2897-2904.
7
8. Erkkilä L, Jauhiainen M, Laitinen K, Haasio K, Tiirola T, Saikku P, et al. Effect of simvastatin, an established lipid-lowering drug, on pulmonary Chlamydia pneumoniae infection in mice. Antimicrob Agents Chemother 2005; 49:3959-3962.
8
9. Stancu C, Sima A. Statins: mechanism of action and effects. J Cell Mol Med 2001; 5:378-387.
9
10. Friesen JA, Rodwell VW. The 3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductases. Genome Biol 2004; 5: 248.
10
11. Jerwood S, Cohen J. Unexpected antimicrobial effect of statins. J Antimicrob Chemother 2008; 61: 362-4.
11
12. Welsh AM, Kruger P, Faoagali J. Antimicrobial action of atorvastatin and rosuvastatin. Pathology 2009; 41:689-691.
12
13. Biradar YS, Jagatap S, Khandelwal KR, Singhania SS. Exploring of antimicrobial activity of triphala mashi an ayurvedic formulation. Evid Based Complement Alternat Med 2008; 5:107-113.
13
14. Begley M, Gahan CG, Hill C. The interaction between bacteria and bile. FEMS Microbiol Rev 2005; 29:625-651.
14
15. Tani H, Sato M, Tsuchiya H, Namikawa I. Cholesterol incorporation into Bacillus megaterium without compositional modification of membrane lipids in response to changes of the membrane functions. Current Microbiol 1993; 26:253-256.
15
16. Kannenberg E, Poralla K. Hopanoid biosynthesis and function in bacteria. Naturwissenschaften 1999; 86:168-176.
16
17. Siedenburg G, Jendrossek D. Squalene-hopene cyclases. Appl Environ Microbiol 2011; 77:3905-15.
17
18. Schmerk CL, Bernards MA, Valvano MA. Hopanoid production is required for low-pH tolerance, antimicrobial resistance, and motility in Burkholderia cenocepacia. J Bacteriol 2011; 193:6712–6723.
18
19. Smith PF, Henrikson CV. Growth inhibition of Mycoplasma by inhibitors of polyterpene biosynthe-sis and its reversal by cholesterol. J Bacteriol 1966; 91:1854-1858.
19
ORIGINAL_ARTICLE
Effects of gamma oryzanol on factors of oxidative stress and sepsis-induced lung injury in experimental animal model
Objective (s): There is corroborating evidence to substantiate redox imbalance and oxidative stress in sepsis that finally leads to organ damage or even death. Gamma oryzanol (GO) is one of the major bioactive components in rice bran has been considered to function as an antioxidant. The present study was carried out to evaluate the antioxidant activity of gamma oryzanol in vitro and its efficacy in sepsis. Materials and Methods: To induce sepsis, cecal ligation and puncture (CLP) method was performed on the rats. A study group of forty male Wistar rats were divided into the following groups: sham group; CLP group; 50 mg/kg GO- treated CLP group and 100 mg/kg GO- treated CLP group. GO was administered with an oral gavage 2 hr prior to inducing sepsis. Tissue and blood samples were collected 12 hr after CLP to prepare tissue sections for histopathological study and assay the oxidative stress biomarkers including: SOD (Superoxide Dismutase), TAC (total antioxidant capacity), MDA (Malondialdehyde), MPO (Myeloperoxidase) and PAI-1 (Plasminogen Activator Inhibitor-1). Data are given as mean ± SD. The ANOVA with Tukey post hoc test was used to determine the differences between groups and P Results: TAC level increased in GO- treated CLP groups (P<0.05). Inflammation score of lung tissue and MPO activity were significantly lower in GO treated CLP group (P<0.05). Conclusion:It seems that GO has a protective effect on lung inflammation and improves the body redox capacity during sepsis.
https://ijbms.mums.ac.ir/article_6283_74af3da1c624c80344b710cb9360a239.pdf
2015-12-01
1257
1263
10.22038/ijbms.2015.6283
CLP
Gamma oryzanol
Oxidative stress
Sepsis
Elmira
Zolali
elmira.zolali@gmail.com
1
Iranian Evidence Based Medicine Center of Excellence, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Parina
Asgharian
parina.asgharian@gmail.com
2
Student Research Committee, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Hamed
Hamishehkar
hamishehkar.hamed@gmail.com
3
Drug Applied Research Center, Pharmaceutics Department, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Maryam
Kouhsoltani
mkoohsoltani@yahoo.com
4
Department of Oral and Maxillofacial Pathology, Faculty of Dentistry, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Hajhir
Khodaii
hazhir.khodaie@gmail.com
5
Iranian Evidence Based Medicine Center of Excellence, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Hadi
Hamishehkar
hamishehkar@tbzmed.ac.ir
6
Drug Applied Research Center, Clinical Pharmacy (Pharmacotherapy) Department, Tabriz University of Medical Sciences, Tabriz, Iran
LEAD_AUTHOR
1. Nguyen HB, Rivers EP, Abrahamian FM, Moran GJ, Abraham E, Trzeciak S, et al. Severe sepsis and septic shock: review of the literature and emergency department management guidelines. Ann Emerg Med 2006; 48:54-e51.
1
2. Chabot F, Mitchell J, Gutteridge J, Evans T. Reactive oxygen species in acute lung injury. Eur Respir J 1998; 11:745-757.
2
3. Gutteridge JMC, Mitchell J. Redox imbalance in the critically ill. Br Medical Bull 1999; 55:49-75.
3
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ORIGINAL_ARTICLE
Contributors (Peer Reviewers)
https://ijbms.mums.ac.ir/article_6294_e754ad24dff36233d037eb8d8a305ca8.pdf
2015-12-01
1264
1265
10.22038/ijbms.2015.6294