ORIGINAL_ARTICLE
Calcitonin Gene-Related Peptide Effects on Phenotype and IL-12 Production of Monocyte-Derived Dendritic Cells in Rheumatoid Arthritis Patients
Objective(s)
Recent studies on human indicate that the introduction of therapeutic use of tolerogenic dendritic cell (DC) for chronic inflammatory conditions is imminent. For the purpose of defining CGRP potency in tolerogenic DC production, we investigated the phenotype and IL-'2 production of DCs generated from the monocytes of rheumatoid arthritis (RA) patients in the presence of the calcitonin gene-related peptide (CGRP), as a multifunctional neuropeptide.
Materials and Methods
DCs were generated from isolated monocytes from four resistant and two early female RA patients using IL- 4, GM-CSF, and CGRP at concentrations of 0, ', and '00 nM. Then, the phenotype of neuropeptide-treated or untreated DCs was determined using flow cytometry and the IL-'2 production was measured by ELISA.
Results
Our study showed that, on the last day of the culture, at a concentration of ' nM CGRP, the mean fluorescence intensity (MFI) for CD80 increased ('4.'3%) and the MFIs for CD83, CD86, and HLA-DR decreased ('4.57%, 5.28%, and 6.88% respectively). Moreover, at '00 nM CGRP concentration, the MFI for CD80 increased (''.'0%) and the MFIs for CD83, CD86, and HLA-DR decreased (4.27%, '8.60%, and '9.75% respectively). In addition, our results indicated that the mean concentrations of IL-'2 produced at 0, ', and '00 nm CGRP concentrations measured '3.72±2.4', ''.0'±'.6', and 7±'.34 pg/ml respectively.
Conclusion
Decreased CD83, CD86, and HLA-DR expression and reduced IL-'2 production by CGRP were found in the RA patients' monocyte-derived DCs. CD83 is a well-defined DC activation marker. HLA-DR and CD86 are appropriate molecules for inducing an immune response. IL-'2 promotes cell-mediated immunity. Therefore we suggest that CGRP may be used as an inducer in the production of tolerogenic DCs.
https://ijbms.mums.ac.ir/article_5108_0873d3ea7064ff37a0367c9a0fb782ad.pdf
2010-10-01
161
169
10.22038/ijbms.2010.5108
Calcitonin gene-related peptide
Dendritic cell
Immune tolerance
Rheumatoid arthritis
Javid
Morad Abbasi
abbasijvd@yahoo.com
1
Immunology Research Center, BuAli Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Maryam
Rastin
2
Immunology Research Center, BuAli Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Zahra
Rezaieyazdi
rezaieyazdiz@mums.ac.ir
3
Rheumatic Diseases Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Zahra
Mirfeizi
rdrc@mums.ac.ir
4
Rheumatic Diseases Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Seyed-Mohammad
Moazzeni
5
Department of Immunology, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran
AUTHOR
Nafise
Tabasi
6
Immunology Research Center, BuAli Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Azam
Brook
7
Immunology Research Center, BuAli Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mahmoud
Mahmoudi
mahoudim @mums.ac.ir
8
Immunology Research Center, BuAli Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1.Kavanaugh A. Economic consequences of established rheumatoid arthritis and its treatment. Best Pract Res Clin Rheumatol 2007; 21:929-942.
1
2.Lutzky V, Hannawi S, Thomas R. Cells of the synovium in rheumatoid arthritis. Dendritic cells. Arthritis Res Ther 2007: 9:219.
2
3.Firestein GS. Immunologic mechanisms in the pathogenesis of rheumatoid arthritis. J Clin Rheumatol 2005; 11:S39-44.
3
4.Panayi GS, Corrigall VM. BiP, an anti-inflammatory ER protein, is a potential new therapy for the treatment of rheumatoid arthritis. Novartis Found Symp 2008; 291:212-216.
4
5.Yamaoka K, Tanaka Y. Jak inhibitor; possibility and mechanism as a new disease modifying anti-rheumatic drug. Nihon Rinsho Meneki Gakkai Kaishi 2009; 32:85-91.
5
6.Rossi M,Young JW.Human dendritic cells: potent antigen-presenting cells at the crossroads of innate and adaptive immunity. J Immunol 2005; 175:1373-1381.
6
7.Steinbrink K, Mahnke K, Grabbe S, Enk AH, Jonuleit H. Myeloid dendritic cell: From sentinel of immunity to key player of peripheral tolerance? Hum Immunol 2009; 70:289-293.
7
8.Thomson AW, Robbins PD. Tolerogenic dendritic cells for autoimmune disease and transplantation. Ann Rheum Dis 2008; 67:iii90-96.
8
9.Manfred B, Lutz GS. Immature, semi-mature and fully mature dendritic cells: which signals induce tolerance or immunity? Trends Immunol 2002; 23:445-451.
9
10.Morelli AE, Thomson AW. Tolerogenic dendritic cells and the quest for transplant tolerance. Nat Rev Immunol 2007; 7:610-621.
10
11.Taub DD. Neuroendocrine interactions in the immune system. Cell Immunol 2008; 252:1-6.
11
12.Wang H, Xing L, Li W, Hou L, Guo J, Wang X. Production and secretion of calcitonin gene-related peptide from human lymphocytes. J Neuroimmunol 2002; 130:155-162.
12
13.Harzenetter, MD, Novotny AR, Gais P, Molina CA, Altmayr F, Holzmann B. Negative regulation of TLR responses by the neuropeptide CGRP is mediated by the transcriptional repressor ICER. J Immunol 2007; 179:607-615.
13
14.Gomes RN, Castro-Faria-Neto HC, Bozza PT, Soares MB, Shoemaker CB, David JR, et al. Calcitonin gene- related peptide inhibits local acute inflammation and protects mice against lethal endotoxemia. Shock 2005; 24:590-594.
14
15.Bracci-Laudiero L, Aloe L, Buanne P, Finn A, Stenfors C, Vigneti E, et al. NGF modulates CGRP synthesis in human B-lymphocytes: a possible anti-inflammatory action of NGF? J Neuroimmunol 2002; 123:58-65.
15
16.Fox FE, Kubin M, Cassin M, Niu Z, Hosoi J, Torii H, et al. Calcitonin gene-related peptide inhibits proliferation and antigen presentation by human peripheral blood mononuclear cells: effects on B7, interleukin 10, and interleukin 12. J Invest Dermatol 1997; 108:43-48.
16
17.Torii H, Hosoi J, Beissert S, Xu S, Fox FE, Asahina A, et al. Regulation of cytokine expression in macrophages and the Langerhans cell-like line XS52 by calcitonin gene-related peptide. J Leukoc Biol 1997; 61:216-223.
17
18.Reyes-Garcia MG, Garcia-Tamayo F. A neurotransmitter system that regulates macrophage pro-inflammatory functions. J Neuroimmunol 2009; 216:20-30.
18
19.Carucci JA, Ignatius R, Wei Y, Cypess AM, Schaer DA, Pope M, et al. Calcitonin gene-related peptide decreases expression of HLA-DR and CD86 by human dendritic cells and dampens dendritic cell-driven T cell- proliferative responses via the type I calcitonin gene-related peptide receptor. J Immunol 2000; 164:3494-3499.
19
20.Seiffert K, Granstein RD. Neuroendocrine regulation of skin dendritic cells. Ann N Y Acad Sci 2006; 1088:195-206.
20
21.Bulloch K,McEwen BS, Nordberg J, Diwa A, Baird S. Selective regulation of T-cell development and function by calcitonin gene-related peptide in thymus and spleen. An example of differential regional regulation of immunity by the neuroendocrine system. Ann N Y Acad Sci 1998; 840:551-62.
21
22.Talme T, Liu Z, Sundqvist KG. The neuropeptide calcitonin gene-related peptide (CGRP) stimulates T cell migration into collagen matrices. J Neuroimmunol 2008; 196:60-66.
22
23.Schlomer JJ,Storey BB,Ciornei RT,McGillis JP. Calcitonin gene-related peptide inhibits early B cell development in vivo. J Leukoc Biol 2007; 81:802-808.
23
24.Foreman JC. Substance P and calcitonin gene-related peptide: effects on mast cells and in human skin. Int Arch Allergy Appl Immunol 1987; 82:366-371.
24
25.Springer J, Geppetti P, Fischer A, Groneberg DA. Calcitonin gene-related peptide as inflammatory mediator. Pulm Pharmacol Ther 2003; 16:121-130.
25
26.Eysselein VE, Reinshagen M, Patel A, Davis W, Nast C, Sternini C. Calcitonin gene-related peptide in inflammatory bowel disease and experimentally induced colitis. Ann N Y Acad Sci 1992; 657:319-327.
26
27.Kroeger I, Erhardt A, Abt D, Fischer M, Biburger M, Rau T, et al. The neuropeptide calcitonin gene-related peptide (CGRP) prevents inflammatory liver injury in mice. J Hepatol 2009; 51:342-353.
27
28.Tang Y, Feng Y, Wang X. Calcitonin gene-related peptide potentiates LPS-induced IL-6 release from mouse peritoneal macrophages. J Neuroimmunol 1998; 84:207-212.
28
29.Liu J, Chen M, Wang X. Calcitonin gene-related peptide-enhanced nitric oxide release and inducible NOS activity and mRNA expression in LPS-stimulated mouse peritoneal macrophages. Shock 2001;16:64-69.
29
30.Yaraee R,Ebtekar M, Ahmadiani A, Sabahi F. Neuropeptides (SP and CGRP) augment pro-inflammatory cytokine production in HSV-infected macrophages. Int Immunopharmacol 2003; 3:1883-1887.
30
31.Sallusto F, Lanzavecchia A. Efficient presentation of soluble antigen by cultured human dendritic cells is maintained by granulocyte/macrophage colony-stimulating factor plus interleukin 4 and downregulated by tumor necrosis factor alpha. J Exp Med 1994; 179: 1109-1118.
31
32.Eskandari F,Webster JI, Sternberg EM. Neural immune pathways and their connection to inflammatory diseases. Arthritis Res Ther 2003; 5:251-265.
32
33.Jara LJ, Navarro C, Medina G, Vera-Lastra O, Blaanco F. Immune-neuroendocrine interactions and autoimmune diseases. Clin Dev Immunol 2006; 13:109-123.
33
34.Ghatta S, Nimmagadda D, Calcitonin gene-related peptide: Understanding its role. Indian Jf Pharmacol 2004; 36:277.
34
35.Nong YH, Titus RG, Ribeiro JM, Remold HG. Peptides encoded by the calcitonin gene inhibit macrophage function. J Immunol 1989; 143:45-49.
35
36.Cao W, Lee SH, Lu J. CD83 is preformed inside monocytes, macrophages and dendritic cells, but it is only stably expressed on activated dendritic cells. Biochem J 2005; 385:85-93.
36
37.Prechtel AT, Steinkasserer A.CD83: an update on functions and prospects of the maturation marker of dendritic cells. Arch Dermatol Res 2007; 299:59-69.
37
38.Sansom DM, Manzotti CN, Zheng Y.What's the difference between CD80 and CD86? Trends Immunol 2003; 24:314-319.
38
39.Perez N, Karumuthil Melethil S, Li R, Praabhakar BS, Holterman MJ, Vasu C. Preferential costimulation by CD80 results in IL-10-dependent TGF-beta1 (+) -adaptive regulatory T cell generation. J Immunol 2008; 180:6566-6576.
39
40.Wing K, Onishi Y, Prieto-Martin P, Yamaguchi T, Miyara M, Fehervari Z, et al. CTLA-4 control over Foxp3+ regulatory T cell function. Science 2008; 322:271-275.
40
41.Salek-Ardakani S, Arens R, Flynn R,Sette A, Schoenbereger SP, Croft M. Preferential use of B7.2 and not B7.1 in priming of vaccinia virus-specific CD8 T cells. J Immunol 2009; 182:2909-2918.
41
42.Suvas S, Singh V, Sahdev S, Vohra H, Agrewala JN. Distinct role of CD80 and CD86 in the regulation of the activation of B cell and B cell lymphoma. J Biol Chem 2002; 277:7766-7775.
42
43.Steinman RM, Hawiger D, Nussenzweig MC. Tolerogenic dendritic cells. Annu Rev Immunol 2003; 21:685-711.
43
44.Capellino S, Straub RH. Neuroendocrine immune pathways in chronic arthritis. Best Pract Res Clin Rheumatol 2008; 22:285-297.
44
ORIGINAL_ARTICLE
Chronic Effects of Di(2-ethylhexyl)phthalate on Stereological Parameters of Testis in Adult Wistar Rats
Objective(s)
In recent years concerns have been raised regarding the incidence of male reproductive disorders from exposure to endocrine disruptors. So, chronic effects of di(2-ethylhexyl)phthalate were studied on histological and stereological structure of testis in adult Wistar rats.
Materials and Methods
Thirty two adult Wistar rats were randomly divided in four equal experiment groups; oil vehicle group and three treated groups which received 10, 100 and 500 mg/kg/day di(2-ethylhexyl)phthalate by gavage for 90 days, respectively. At the end of exposure period the volume of testes was measured by Cavellieri method, testes weight was recorded and then fixed in Bouin’s solution. Following tissue processing, 5 pm sections were stained with haematoxylin-eosin and evaluated with quantitative techniques. Seminiferous tubule diameter, germinal epithelium height, relative and total volumes of seminiferous tubules, tubular lumen and interstitial tissue were estimated.
Results
The results showed that mean weight and volume of testis were decreased significantly (35.2% and 23.9% respectively) in rats treated with 500 mg/kg/day DEHP for 90 days. Seminiferous tubules diameter reduced, 4.4% and 13.4% in 100 and 500 mg/kg/day DEHP-treated groups, respectively. Relative volumes of tubular lumen and interstitial tissue were increased significantly in 100 (P< 0.05) and 500 (P< 0.01) mg/kg/day doses groups. Also, testosterone serum levels were significantly higher (P< 0.05) in rats exposed to 500 mg/kg/day DEHP.
Conclusion
Present study indicated dose-dependent reductions of testicular parameters in adult male rats chronically exposed to di(2-ethylhexyl)phthalate.
https://ijbms.mums.ac.ir/article_5109_77ff022f80cbe86f6fdeb9e1bc1d24f2.pdf
2010-10-01
170
176
10.22038/ijbms.2010.5109
Di(2-ethylhexyl)phthalate
Spermatogenesis
Stereology
Testis
Mehran
Dorostghoal
mdorostghoal@yahoo.com
1
Department of Biology, Faculty of Sciences, Shahid Chamran University of Ahwaz, Ahwaz,
LEAD_AUTHOR
Adel
Zardkaf
2
Department of Biology, Faculty of Sciences, Shahid Chamran University of Ahwaz, Ahwaz,
AUTHOR
Abdolrahaman
Dezfoolian
3
Department of Anatomical Sciences, Faculty of Medicine, Jondishapour Medical Sciences University of Ahwaz, Ahwaz, Iran
AUTHOR
1.Brake A, Krause W. Decreasing quality of semen. BMJ 1992; 305:1498.
1
2.Suresh C, Sikka RW. Endocrine disruptors and estrogenic effects on male reproductive axis. Asian J Androl 2008; 10:134-145.
2
3.Kurahashi N, Kondo T, Omura M, Umemura T, Ma M, Kishi R. The effects of subaccute inhalation of Di(2- ethylhexyl) Phthalate on the testes of prepupertal wistar rats. J Occup Health 2005; 47:437-444.
3
4.Akingbemi BT, Youker RT, Sottas CM, Ge R, Katz E, Klinefelter GR, et al. Modulation of rat Leydig cell steroidogenic function by di(2-ethylhexyl)phthalate. Biol Reprod 2001; 65:1252-1259.
4
5.Arcadi FA, Costa C, Imperatore C, Marchese A, Rapisardi A, Salemi M, et al. Oral toxicity of di(2- ethylhexyl)phthalate during pregnancy and suckling in the Long-Evans rat. Food Chem_Toxicol 1998; 963-97.
5
6.Poon R, Lecavaliert P, Mueller R, Valli VE, Procter BG, Chu I. Subchronic oral toxicity of di(n-octyl) phthalate and di(2-ethylhexyl) phthalate in the rat. Food Chem Toxicol 1997; 35:225-239.
6
7.David RM, Moore MR, Finney DC, Guest D. Chronic toxicity of di(2-ethylhexyl)phthalate in rats. Toxicol Sci 2000; 55:433-443.
7
8.Lamb JC, Chapin RE, Teague J, Lawton AD, Reel JR. Reproductive effects of four phthalic acid esters in the mouse. Toxicol Appl Pharmacol 1987; 88:55-269.
8
9.Ge RS, Chen GR, Dong Q, Akingbemi B, Sottas CM, Santos M, et al. Biphasic effects postnatal exposure to di(2-ethylhexyl) phthalate on the timing of puberty in male rats. J Androl 2007; 28: 513-520.
9
10.Sprando RL. Perfusion of the rat testis through the heart using heparin. In: Russell LD, Ettlin RA, Sinha HAP, Clegg ED, editors. Histological and Histopathological Evaluation of the Testis. Clearwater: Cache River Press; 1990. p. 277-280.
10
11.Howard CV, Reed MG. Unbiased Stereology. Guilford: Bios Scientific Publishers; 1998.
11
12.Creasy DM, Foster JR, Foster PMD. The morphological development of di (n-penthyl) phthalate induced testicular atrophy in the rat. J Pathol 1983; 139:309-321.
12
13.Gray TJB, Gangoli SD. Aspects of the testicular toxicity of Phthalate esters. Environ Health Piespect 1986; 65:229-235.
13
14.Oishi S. Prevention of di(2-ethylhexyl)phthalate-induced testicular atrophy in rats by co-administration of the vitamin B12 derivative adenosylcobalamin. Arch Environ Contam Toxicol 1994; 26:497-503.
14
15.Rhodes C, Orton TC, Pratt IS. Compartive pharmaocokinetics and subacute toxicity of di(2- ethylhexyl)phthalate in rats and marmosets: Extrapolation of effects in rodents to man. Environ Health Perspect 1986; 65:299-308.
15
16.Parmar D, Srivastava SP, Singh GB, Seth PK. Effect of testosterone on the testicular atrophy_caused by di(2- ethylhexyl) phthalate (DEHP). Toxicol Lett 1987; 36:297-308.
16
17.Klimisch HJ, Gamer AO, Hellwig J, Kaufmann W, Jackh R. di(2-ethylhexyl)phthalate (DEHP): A short-term repeated inhalation toxicity study including fertility assessment. Food Chem_Toxic 1992; 30: 915-919.
17
18.Pugh G, Isenberg JS, Kamendulis LM, Ackley DC, Clare LJ, Brown R, et al. Effects of Di (isononyl) Phthalate, di(2-ethylhexyl)phthalate, and Clofibrate in cynomolgous monkeys. Toxicol_Sci 2000; 56:181-188.
18
19.Sjoberg P, Bondesson U, Gray TJB, Ploen L. Effects of di(2-ethylhexyl)phthalate and five of its metabolites on rat testis in vivo and in vitro. Acta Pharmacol Toxicol 1986; 58:225-233.
19
20.Zacharewski TR, Meek MD, Clemons JH, Wu ZF, Fielden MR, Matthews JB. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Toxicol Sci 1998; 46:282-293.
20
21.Gray LE, Kelce WR, Wiese T, Tyl R, Gaido K, Cook J, et al. Endocrine screening methods workshop report: detection of estrogenic and androgenic hormonal and antihormonal activity for chemicals that act via receptor or steroidogenic enzyme mechanisms. Reprod Toxicol 1997; 11: 719-750.
21
22.Akingbemi BT, Ge R, Klinefelter GR, Zirkin BR, Hardy PM. Phthalate-induced Leydig cell hyperplasia is associated with multiple endocrine disturbances. PNAS 2004; 101: 775-780.
22
23.Hardy MP, Gelber SJ, Zhou ZF, Penning TM, Ricigliano JW, Ganjam VK, et al. Hormonal control of Leydig cells differentiation. Ann N Y Acad Sci 1991; 637:152-163.
23
24.Oishi S, Higara K. Effect of phthalic acid esters on gonadal function in male rats. Bull Environ Contam Taxicol 1979; 21:65-67.
24
25.Ljungvall K, Karlsson P, Hulten F, Madej A, Norrgren L, Einarsson S, et al. Delayed effects on plasma concentration of testosterone and testicular morphology by intramuscular low-dose di(2-ethylhexyl)phthalate or estradiol benzoate in the prepubertal boar. Theriogenology 2005; 64: 1170-1184.
25
26.Foster PM, Mylchreest E, Gaido KW, Sar M. Effects of phthalate esters on the developing reproductive tract of male rats. Hum Reprod Update 2001; 7:231-235.
26
27.Shultz VD, Phillips S, Sar M, Foster PM, Gaido KW. Analysis of altered gene expression profiles in fetal rat testis exposed to di (n-butyl) phthalate in utero using cDNA arrays. Taxicol Sci 2001; 64:233-242.
27
ORIGINAL_ARTICLE
Antioxidant Enzymes and Acute Phase Proteins Correlate with Marker of Lipid Peroxide in Adult Nigerian Sickle Cell Disease Patients
Objective(s)
Sickle cell disease is a genetic disorder characterized by chronic haemolytic anaemia. Haemoglobin S containing red blood cells may be susceptible to oxidative stress due to imbalance between production of reactive oxygen species and the countering effect of the various antioxidants present in the body.
Materials and Methods
We evaluated some antioxidant enzymes which include glutathione peroxidase, superoxide dismutase, and catalase. We also determined malondialdehyde, C- reactive protein and fibrinogen using commercial kits in 144 adult sickle cell disease patients (68 males and 76 females) in steady state and 80 apparently healthy age/sex matched controls; 40 sickle cell trait (20 males/20 females) and 40 normal haemoglobin (20 males/20 females).
Results
The result showed that serum glutathione peroxidase, superoxide dismutase and catalase were lower in sickle cell disease patients compared with controls. Malondialdehyde, C-reactive protein and fibrinogen were significantly increased in sickle cell disease patients compared to the controls in both sexes. Malondialdehyde correlated negatively with superoxide dismutase (P< 0.01), glutathione peroxidase (P< 0.05), and catalase (P< 0.05) and positively (P< 0.05) with C - reactive protein and fibrinogen.
Conclussion
This study shows that malondialdehyde correlated negatively with antioxidant enzymes and positively with acute phase proteins in sickle cell anaemia patients in steady state.
https://ijbms.mums.ac.ir/article_5110_de9724ea8262f65a3d14c17e4d2a764f.pdf
2010-10-01
177
182
10.22038/ijbms.2010.5110
Acute phase protein
Antioxidant Enzymes
Malondialdehyde
Sickle cell disease
Abiodun
Mathias Emokpae
biodunemokpae@yahoo.com
1
Department of Chemical Pathology, Aminu Kano Teaching Hospital, PMB 3452, Kano, Nigeria
LEAD_AUTHOR
Uadia
Patrick Ojiefo
2
Department of Biochemistry, University of Benin, Benin city, Nigeria.
AUTHOR
Kuliya-Gwarzo
Aisha
3
Department of Haematology and Blood Transfusion, Aminu Kano Teaching Hospital, Kano, Nigeria
AUTHOR
1.Beyer JE, Simon LE. Home treatment of pain for children and adolescents with sickle cell disease. Pain Manag Nurs 2004; 5:126-135.
1
2.Steinberg MH. Pathophysiologically based drug treatment of sickle cell disease. Trends Pharmacol Sci 2006; 27:204-210.
2
3.Hebbel RP, Eaton JW, Balasingam M, Steinberg MH. Spontaneous oxygen radical generation by sickle erythrocytes. J clin Invest 1982; 70:1253-1259.
3
4.Kings ES, Farber HW. Role of free radicals in the pathogenesis of acute chest syndrome in sickle cell disease. Respir Res 2001; 2:280-285.
4
5.Airede KJ, Ibrahim M. Antioxidants in Neonatal systemic disease. Sahel Med J 1999; 2:66-72.
5
6.Yam J, Frank L, Roberts RJ. Oxygen toxicity: comparison of lung biochemical response in neonatal and adult rats. Pediatr Res 1978; 12:115-119.
6
7.Fridovich I, Freeman B. Antioxidant defences in the lung. Annu Rev Physiol 1986; 48:693-697.
7
8.Halliwell B, Gutteridge JMC. Cellular responses to oxidative stress: adaptation, damage, repair, senescence and death in: Halliwell B, Gutteridge JMC eds. Free radicals in Biology and Medicine. 3rd ed. New York: Oxford university press; 2007.p.187-267.
8
9.Fasola F, Adedapo K, Anetor J, Kuti M. Total Antioxidant status and some hematological values in sickle cell disease patients in steady state. J Natl Med Assoc 2007; 99:891-894.
9
10.Arinola OG, Olaniyi JA, Akinbinu MO. Evaluation of antioxidant levels and trace elements status in Nigerian sickle cell disease patients with plasmodium parasitaemia. Pak J Nutr 2008; 7:766-769.
10
11.Burmester K, Aulton K, Horsfield GI. Evaluation of a rapid method for the determination of plasma fibrinogen. J Clin Pathol 1970; 23:43-46.
11
12.Chiu D, Lubin B. Abnormal vitamin E and glutathione peroxidase levels in sickle cell anaemia: evidence for increased susceptibility to lipid peroxidation in vivo. J Lab Clin Med 1979; 94:542-548.
12
13.Das SK, Nair RC. Superoxide dismutase, glutathione peroxidase, catalase and lipid peroxidation of normal and sickled erythrocytes. Br J Haematol 1980; 44:87-92.
13
14.Asian M, Thornley-Brown D, Freeman BA. Reactive species in sickle cell disease. Ann N Y Acad Sci 2000; 899:375-391.
14
15.Manfredini V, Lazzaretti LL, Griebeler IH, Santin AP, Brandao VD, Wagner S, et al. Blood antioxidant parameters in sickle cell anaemia patients in steady state. J Natl Med Assoc 2008; 100:897-902.
15
16.Takasu J, Uykimpang R, Sunga MA, Amagase H, Nihara Y. Aged garlic extract therapy in sickle cell anaemia patients. BMC Blood Disorders 2002; 2:3.
16
17.Antunes F, Salvador A, Marinho HS, Alves R, Pinto RE. Lipid peroxidation in mitochondrial inner membranes I. An integrative kinetic model. Free Radic Biol Med 1996; 21:917-943.
17
18.Pawlak K, Pawlek D, Mysliwice M. Cu/Zn superoxide dismutase plasma levels as a new useful chemical biomarker of oxidative stress in patients with end stage renal disease Clin Biochem 2005; 38:700-705.
18
19.Bourantas KL, Dalekos GN, Makis A, Chaidos A, Tsiara S, Mavridis A. Acute phase proteins and interleukins in steady state sickle cell disease. Eur J Haematol 1998; 61:49-54.
19
20.Svarch E, Hernandez P, Ballester JM. Sickle cell disease in cuba; general review,Institute de Hematologia en Immunologia (IHI) la Havana, Cuba 2001.
20
ORIGINAL_ARTICLE
Comparative Molecular and Microbiologic Diagnosis of Vaginal Colonization by Group B Streptococcus in Pregnant Women during Labor
Objective(s)
Rapid tests for detection of Streptococcus agalactiae or Group B Streptococci (GBS) at the onset of labor are needed to permit early intrapartum antibiotic prophylaxis. This study aimed to evaluate the PCR assays targeting the 16S ribosomal RNA gene (16S rDNA) for detection of the GBS in comparison with a specific culture method.
Materials and Methods
Two swabs were used to obtain vaginal specimens from the 330 pregnant women attended delivery room at Hedayat hospital, Tehran, Iran. One swab was analyzed by direct plating onto selective GBS agar medium (ISLAM) and the other swab was used for a PCR assay, which amplified the 16S rDNA of S. agalactiae. Comparative study between the selective culture and the PCR assay was done among the 330 tested women. Results
The GBS colonization rate based on the culture results was 20.6% (68/330). Both culture and PCR methods were positive for 56 and negative for 253 women. The culture method was positive and PCR was negative in 12 women. The culture was negative and the PCR positive for 9 women. Sensitivity of the PCR assay was 82.3% and specificity was 96.5%. The positive predictive value was 86.15% and negative predictive value was 95.4%.
Conclusion
ISLAM diagnostic procedure and PCR are rapid and reliable analyzing methods, which might be useful for accurate diagnosis of GBS colonization in pregnant women at the time of delivery.
https://ijbms.mums.ac.ir/article_5111_8f57fbfa49c9c2c7cc39219108dd732f.pdf
2010-10-01
183
188
10.22038/ijbms.2010.5111
Early diagnosis
PCR
rRNA gene
Streptococcus agalactiae
Streptococcal infection
Farnaz
Fatemi
1
Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR, Tehran, Iran
AUTHOR
Parviz
Pakzad
2
Department of Microbiology, Islamic Azad University, North of Tehran Branch, Tehran, Iran
AUTHOR
Hojjat
Zeraati
3
Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Saeed
Talebi
4
Monoclonal Antibody Research Center, Avicenna Research Institute, ACECR, Tehran, Iran
AUTHOR
Soheila
Asgari
5
International Campus, Tehran University of Medical Sciences, Kish, Iran
AUTHOR
Mohammad-Mehdi
Akhondi
6
Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR, Tehran, Iran
AUTHOR
Leili
Chamani-Tabriz
lchamani@gmail.com
7
Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR, Tehran, Iran
LEAD_AUTHOR
1.Brooks GF, Butel JS, Morse SA. Jawetz, Melnick, & Adelberg's medical microbiology. 23rd.ed. New York: London: Lange Medical Books/McGraw Hill; 2004.
1
2.Cunningham FG, Williams JW. Williams obstetrics. 22nd ed. New York: McGraw-Hill Medical; 2005.
2
3.CDC. Prevention of perinatal group B streptococcal disease: a public health perspective. Centers for Disease Control and Prevention. MMWR Recomm Rep 1996; 45:1-24.
3
4.Schuchat A. Epidemiology of group B streptococcal disease in the United States: shifting paradigms. Clin Microbiol Rev 1998; 11:497-513.
4
5.Schrag S, Gorwitz R, Fultz-Butts K, Schuchat A. Prevention of Perinatal Group B Streptococcal Disease. MMWR Recomm Rep 2002; 51:1-22.
5
6.Boyer KM, Gadzala CA, Burd LI, Fisher DE, Paton JB, Gotoff SP. Selective intrapartum chemoprophylaxis of neonatal group B streptococcal early-onset disease. I. Epidemiologic rationale. J Infect Dis 1983; 148:795-801.
6
7.Anukam KC, Osazuwa EO, Ahonkhai I, Reid G. Assessment of Lactobacillus species colonizing the vagina of apparently healthy Nigerian women, using PCR-DGGE and 16S rRNA gene sequencing. World J Microbiol Biotechnol 2006; 22:1055-1060.
7
8.Burton JP, Reid G. Evaluation of the bacterial vaginal flora of 20 postmenopausal women by direct (Nugent score) and molecular (polymerase chain reaction and denaturing gradient gel electrophoresis) techniques. J Infect Dis 2002; 186:1770-1780.
8
9.Anukam KC, Reid G. Organisms associated with bacterial vaginosis in Nigerian women as determined by PCR- DGGE and 16S rRNA gene sequence. Afr Health Sci 2007; 7:68-72.
9
10.Riffon R, Sayasith K, Khalil H, Dubreuil P, Drolet M, Lagace J. Development of a rapid and sensitive test for identification of major pathogens in bovine mastitis by PCR. J Clin Microbiol 2001; 39:2584-2549.
10
11.Giovannoni SJ, DeLong EF, Olsen GJ, Pace NR. Phylogenetic group-specific oligodeoxynucleotide probes for identification of single microbial cells. J bacteriol 1988; 170:720-726.
11
12.Bentley RW, Leigh JA. Determination of 16S ribosomal RNAgene copy number in Streptococcus uberis, S. glaciate, S. dysgalactiae and S. parauberis. FEMS Immunol Med Microbiol 1995; 12:1-7.
12
13.Barcaite E, Bartusevicius A, Tameliene R, Kliucinskas M, Maleckiene L, Nadisauskiene R. Prevalence of maternal group B Streptococcal colonisation in European countries. Acta Obstet Gynecol Scand 2008; 87:260-271.
13
14.Valkenburg-van den Berg AW, Sprij AJ, Oostvogel PM, Mutsaers JA, Renes WB, Rosendaal FR, et al. Prevalence of colonisation with group B Streptococci in pregnant women of a multi-ethnic population in The Netherlands. Eur J Obstet Gynecol Reprod Biol 2006; 124:178-183.
14
15.Bergeron MG, Ke D, Menard C, Picard FJ, Gagnon M, Bernier M, et al. Rapid detection of group B Streptococci in pregnant women at delivery. N Engl J Med 2000; 343:175-179.
15
16.Atkins KL, Atkinson RM, Shanks A, Parvin CA, Dunne WM, Gross G. Evaluation of polymerase chain reaction for group B Streptococcus detection using an improved culture method. Obstet Gynecol 2006; 108:488-491.
16
17.Votava M, Tejkalova M, Drabkova M, Unzeitig V, Braveny I. Use of GBS media for rapid detection of group B streptococci in vaginal and rectal swabs from women in labor. Eur J Clin Microbiol Infect Dis 2001; 20:120-122.
17
18.Stoll BJ, Schuchat A. Maternal carriage of group B Streptococci in developing countries. Pediatr Infect Dis J 1998; 17:499-503.
18
19.Rabiee S, Arab M, Mashouf R. Epidemiologic pattern of vaginal colonization by group B Streptococcus in pregnant women in Hamadan, Central west of Iran. Iran J Med Sci 2006; 31:106-168.
19
20.Aali BS, Abdollahi H, Nakhaee N, Davazdahemami Z, Mehdizadeh A. The association of preterm labor with vaginal colonization of group B streptococci. IJRM 2007; 5:191-194.
20
21.Namavar Jahromi B, Poorarian S, Poorbarfehee S. The prevalence and adverse effects of group B Streptococcal colonization during pregnancy. Arch Iran Med 2008; 11:654-657.
21
22.Nakhaei Moghaddam M. Recto-Vaginal colonization of Group B Streptococcus in pregnant women referred to a hospital in Iran and its effect on Lactobacillus normal flora. J Biol Sci 2010; 10:166-169.
22
23.Persson E, Berg S, Trollfors B, Larsson P, Ek E, Backhaus E, et al. Serotypes and clinical manifestations of invasive group B Streptococcal infections in western Sweden 1998-2001. Clin Microbiol Infect 2004; 10:791-796.
23
24.Lyytikainen O, Nuorti JP, Halmesmaki E, Carlson P, Uotila J, Vuento R, et al. Invasive group B Streptococcal infections in Finland: a population-based study. Emerg Infect Dis 2003; 9:469-473.
24
25.Phares CR, Lynfield R, Farley MM, Mohle-Boetani J, Harrison LH, Petit S, et al. Epidemiology of invasive group B Streptococcal disease in the United States, 1999-2005. JAMA 2008; 299:2056-2065.
25
26.Ke D, Menard C, Picard FJ, Boissinot M, Ouellette M, Roy PH, et al. Development of conventional and real-time PCR assays for the rapid detection of group B Streptococci. Clin Chem 2000; 46:324-331.
26
27.Gil EG, Rodriguez MC, Bartolome R, Berjano B, Cabero L, Andreu A. Evaluation of the Granada agar plate for detection of vaginal and rectal group B Streptococci in pregnant women. J Clin Microbiol 1999; 37:2648-2651.
27
28.Islam AK. Rapid recognition of group-B Streptococci. Lancet 1977; 1:256-257.
28
29.Miranda C, Ga'mez MI, Navarro JM, Rosa-Fraile M. Endocarditis caused by nonhemolytic group B Streptococcus. J Clin Microbiol 1997; 35:1016-1017.
29
30.Cueto M, Sa'nchez MJ, Serrano J, Aguilar JM, Martinez R, Rosa M. Bacteremia caused by nonhemolytic group B Streptococci. Clin Microbiol Newsl 1996; 18:55-56.
30
31.Dmitriev A, Suvorov A, Shen AD, Yang YH. Clinical diagnosis of group B Streptococci by scpB gene based PCR. Indian J Med Res 2004; 119:233-236.
31
ORIGINAL_ARTICLE
Molecular Cloning, Expression and Purification of Protein TB10.4 Secreted by Mycobacterium Tuberculosis
Objective(s)
Tuberculosis (TB) is the leading cause of mortality among the infectious diseases, especially in developing countries. One of the main goals in tuberculosis research is to identify antigens which have the ability of inducing cellular and/or humoral immunity in order to use them in diagnostic reagents or vaccine design. The aim of this study was to clone and express the TB'0.4 protein in Escherichia coli expression system. Materials and Methods
DNA was extracted from Mycobacterium tuberculosis H37Rv. Gene specific primers were designed using Gene Runner software according to sanger sequence database. Gene tb'0.4 fragment was amplified by PCR method and purified tb'0.4 gene was cloned into pET 102/D vector. Plasmid containing pET102/D-10.4 was transformed into competence E. coli TOP'0. A positive transformant was chosen and plasmids DNA was isolated and subsequently transformed into competence E. coli BL2'(DE3). The bacterium was induced by IPTG and its lysates were loaded directly onto SDS-PAGE. Purified recombinant protein was achieved using metal affinity chromatography (Ni-nitrilotriacetic acid).
Results
TB'0.4 molecule was successfully cloned, expressed, and purified. An approximately 26.4 kDa exogenous protein was observed on the SDS-PAGE. The recombinant protein was confirmed by DNA sequencing of correct insert.
Conclusion
The success of expressing the TB'0.4 protein could serve as a basis for further studies on the usefulness of the gene and its expression product in the development of subunit vaccine and diagnostic method.
https://ijbms.mums.ac.ir/article_5112_9a8e6c2f1e1eaf6692230d3b69d99034.pdf
2010-10-01
189
193
10.22038/ijbms.2010.5112
Gene tb'0.4
Molecular Cloning
Mycobacterium tuberculosis
Protein TB'0.4
Aida
Gholoobi
gholoubiad@mums.ac.ir
1
Microbiology & Virology Research Centre, Bu- Ali Research Institute, Mashad University of Medical Sciences, Mashad, Iran
AUTHOR
Mojtaba
Sankian
2
Division of Immunobiochemistry, Immunology Research Centre, Bu- Ali Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Reza
Zarif
3
Microbiology & Virology Research Centre, Bu- Ali Research Institute, Mashad University of Medical Sciences, Mashad, Iran
AUTHOR
Zahra
Farshadzadeh
4
Microbiology & Virology Research Centre, Bu- Ali Research Institute, Mashad University of Medical Sciences, Mashad, Iran
AUTHOR
Forugh
Youssefi
5
Microbiology & Virology Research Centre, Bu- Ali Research Institute, Mashad University of Medical Sciences, Mashad, Iran
AUTHOR
Ali
Sadeghian
sadeghiana@mums.ac.ir
6
Microbiology & Virology Research Centre, Bu- Ali Research Institute, Mashad University of Medical Sciences, Mashad, Iran
LEAD_AUTHOR
Mohammad
Derakhshan
7
Microbiology & Virology Research Centre, Bu- Ali Research Institute, Mashad University of Medical Sciences, Mashad, Iran
AUTHOR
Abdol-Reza
Varasteh
8
Division of Immunobiochemistry, Immunology Research Centre, Bu- Ali Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
1.Bloom BR, Murray CJ. Tuberculosis: commentary on a emergent killer. Science 1992; 257:1055-1064.
1
2.Global tuberculosis control-surveillance, planning, financing. WHO report. 2006. Available at: http//:www.who.int/tb/publications/global_report/en/index.html. Accessed Jan 2008.
2
3.Doherty TM. Real world TB vaccines: clinical trials in TB-endemic regions. Vaccine 2005; 23:2109-2114.
3
4.Wang J, Xing Z. Tuberculosis vaccines: the past, present and future. Expert Rev Vaccines 2002; 1:341-354. Review.
4
5.Weldingh k, Rosenkrand I, Okkles LM, Doherty TM, Andersen P. Assessing the serodiagnostic potential of 35 Mycobacterium tuberculosis proteins and identification of four navel serological antigens. J Clin Microbiol 2005; 43:57-65.
5
6. Young DB, Kaufmann SH, Hermans PW, Thole JE. Mycobacterial protein antigens: a compilation. Mol. Microbiol. 1992; 6:133-145.
6
7.Andersen P, Askgaard D, Ljungqvist L, Bentzon MW, Heron I. T-cell proliferative response to antigens secreted by Mycobacterium tuberculosis. Infect Immun 1991; 9:1558-1563.
7
8.Andersen P, Heron I. Specificity of a protective memory immune response against Mycobacterium tuberculosis. Infect Immun 1993; 61:844-851.
8
9.Horwitz MA, Lee BW, Dillon BJ, Harth G. Protective immunity against tuberculosis induced by vaccination with major extracellular proteins of Mycobacterium tuberculosis. Proc Natl Acad Sci USA 1995; 92:1530-1534.
9
10.Hubbard RD, Flory CM, Collins FM, Cocito C. Immunization of mice with mycobacterial culture filtrate proteins. Clin Exp Immunol 1992; 88:94-98.
10
11.Orme IM, Andersen P, Boom WH. T cell response to Mycobacterium tuberculosis. J Infect Dis 1993; 167:1481-1497.
11
12.Roberts AD, Sonnenberg MG, Ordway DJ, Furney SK, Brennan PJ, Belisle JT, et al. Characteristics of protective immunity engendered by vaccination of mice with purified culture filtrate protein antigens of Mycobacterium tuberculosis. Immunology 1995; 85:502-508.
12
13.Haslov K, Andersen A, Nagai S, Gottschau A, Sorensen T, Andersen P. Guinea pig cellular immune responses to proteins secreted by Mycobacterium tuberculosis. Infect Immun 1995; 63:804-810.
13
14.Bassey EO, Catty D, Kumararatne DS, Raykundalia C. Candidate antigens for improved serodiagnosis of tuberculosis. Tuber Lung Dis 1996; 77:136-145.
14
15.Havlir DV, Wallis RS, Boom WH, Daniel TM, Chervenak K, Ellner JJ. Human immune response to Mycobacterium tuberculosis antigens. Infect Immun 1991; 59:665-670.
15
16.Kato-Maeda M, Rhee JT, Gingeras TR, Salamon H, Drenkow J, Smittipat N, et al. Comparing genomes within the species Mycobacterium tuberculosis. Genome Res 2001;11:547-554.
16
17.Skjot RLV, Brock I, Arend SM, Munk ME, Theisen M, Ottenhoff THM, et al. Epitope mapping of the immunodominant antigen TB10.4 and the two homologous proteins TB10.3 and TB12.9 which constitute a subfamily of the esat6 gene family. Infect Immun 2002; 70:5446-5453.
17
18.Skjot RLV, Oettinger T, Rosenkrands I, Ravn P, Brock I, Jacobsen S, et al. Comparative evaluation of low molecular mass proteins from Mycobacterium tuberculosis identifies members of the ESAT-6 family as immunodominant T cell antigens. Infect Immun 2000; 68:214-220.
18
19.Dietrich J, Aagaard C, Leah R, Olsen AW, Stryhn A, Doherty TM, et al. Exchanging ESAT-6 with TB10.4 in an Ag85B fusion molecule-based tuberculosis subunit vaccine: efficient protection and ESAT-6 based sensitive monitoring of vaccine efficacy. J Immunol 2005; 174:6332-6339.
19
20.Majlessi L, Rojas MJ, Priscille B, Leclerc C. CD8+ T-cell responces of mycobacterium infected mice to a newly identified major histocompatibility complex class I -restricted epitope shared by proteins of the ESAT-6 family. Infect Immun 2003; 71:7173-7177.
20
21. Hervas-Stubbs S, Majlessi L, Simsova M, Morova J, Rojas MJ, Nouze C, et al. High frequency of CD4+ T- cells specific for the TB10.4 protein correlates with protection against Mycobacterium tuberculosis infection. Infect Immun 2006; 74:3396-3407.
21
22.Johnson BH, Hecht MH. Recombinant proteins can be isolated from Escherichia coli cells by repeated cycles of freezing and thawing. Biotechnology 1994; 12:1357-1360.
22
ORIGINAL_ARTICLE
Study of Nonenzymatic Glycation of Transferrin and its Effect on Iron -Binding Antioxidant Capacity
Objective(s)
Nonenzymatic glycosylation (glycation) occurs in many macromolecules in aging and diabetes due to exposure of biomolecules to high level of glucose. Glycation can changes function, activities and structure of many biomolecules. Considering this important role of transferrin (Trf) in iron transport and antioxidant activity in plasma this study was carried out to investigate the effect of glycation in these processes. Materials and Methods
In this study, human apo-Trf (5 mg/ml in sodium phosphate buffer pH= 7.4) was treated with different concentrations of glucose in different period of times (10 days and 20 days). Rate of glycation was measured using thiobarbituric acid method. The effect of glycation on iron binding antioxidant capacity of apo-Trf was investigated using two methods (RBC hemolysis and fluorescent).
Results
Result showed that rate of glycation of apo-Trf was increased with increase in glucose concentration and time of incubation (P< 0.05). Lower iron binding antioxidant capacity was observed for glycted Trf as compared to native Trf (P< 0.05).
Conclusion
Impairment of antioxidant capacity of glycated Trf can suggest a relationship between glycation of Trf and oxidative stress that occurs due to hyperglycemia in diabetic patients.
https://ijbms.mums.ac.ir/article_5113_e322a166609502b532aed22e8c7060f7.pdf
2010-10-01
194
199
10.22038/ijbms.2010.5113
Apotransferrin
Diabetes Mellitus
Glycation
Oxidative stress
Mohammad Taghi
Goodarzi
mtgoodarzi@yahoo.com
1
Research Center for Molecular Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
LEAD_AUTHOR
Mojtaba
Rashidi
2
Dept of Biochemistry, Medical School, Hamadan University of Medical Sciences, Hamadan, Iran
AUTHOR
Mohsen
Rezaei
drmrezaei@hotmail.com
3
Dept of Biochemistry, Medical School, Hamadan University of Medical Sciences, Hamadan, Iran
AUTHOR
1.Misciagna G, De Michele G, Trevisan M. Non enzymatic glycated proteins in the blood and cardiovascular disease. Curr Pharm Des 2007; 13:3688-3695.
1
2.Nakajou K, Watanabe H, Kragh-Hansen U, Maruyama T, Otagiri M. The effect of glycation on the structure, function and biological fate of human serum albumin as revealed by recombinant mutants. Biochim Biophys Acta 2003; 1623:88-97.
2
3.Kennedy DM, Skillen AW, Self CH. Glycation of monoclonal antibodies impairs their ability to bind antigen. Clin Exp Immunol 1994; 98:245-251.
3
4.Goodarzi MT, Rezaei M, Piry H, Amiry S. Effect of in vitro glycation of human placental collagen (Type IV) on platelet aggregation. Pak J Biolig Sci 2005; 8:1203-1206.
4
5.Goodarzi MT, Ghahramany S, Mirmoemeni MH. Glycation of human IgG induces structural alterations leading to changes in interaction with anti-IgG. Iran J Immunol 2005; 2:36-42.
5
6.Goodarzi MT, Ghahramany S, Mirmoemeni MH. In vitro glycation of human IgG and its effect on interaction with anti-IgG. Iran J Allergy Asthma Immunol 2004; 3:181-187.
6
7.Hemadi M, Kahn PH, Miquel GEl Hage Chahine JM. Transferrin’s mechanism of interaction with receptor 1. Biochemistry 2004; 43:1736-1745.
7
8.Paez PM, Marta CB, Moreno MB, Soto EF, Pasquini JM. Apotransferrin decreases migration and enhances differentiation of oligodendroglial progenitor cells in an in vitro system. Dev Neurosci 2002; 24:47-58.
8
9.Gomme PT, McCann KB, Bertolini J. Transferrin: structure, function and potential therapeutic actions. Drug Discov Today 2005; 10:267-273.
9
10.Van Campenhout A, Van Campenhout C, Lagrou AR, Moorkens G, De Block C, Manuel-y-Keenoy B. Iron-binding antioxidant capacity is impaired in diabetes mellitus. Free Radic Biol Med 2006; 40:1749-1755.
10
11.Negre-Salvayre A, Coatrieux C, Ingueneau C, Salvayre R. Advanced lipid peroxidation end products in oxidative damage to proteins. Potential role in diseases and therapeutic prospects for the inhibitors. Br J Pharmacol 2008; 153:6-20.
11
12.Gallou G, Ruelland A, Campion L, Maugendre D, Le Moullec N, Legras B, et al. Increase in thiobarbituric acid-reactive substances and vascular complications in type 2 diabetes mellitus. Diabete Metab 1994: 20:258¬264.
12
13.Gutteridge JM, Rowley DA, Halliwell B. Superoxide-dependent formation of hydroxyl radicals and lipid peroxidation in the presence of iron salts. Detection of ‘catalytic’ iron and antioxidant activity in extracellular fluids. Biochem J 1982: 206:605-609.
13
14.Gutteridge JM, Quinlan GJ. Antioxidant protection against organic and inorganic oxygen radicals by normal human plasma: the important primary role for iron-binding and iron-oxidizing proteins. Biochim Biophys Acta 1992; 1159:248-254.
14
15.Huebschmann AG, Regensteiner JG, Vlassara H, Reusch JEB. Diabetic and advanced glycoxidation end products. Diabetes Care 2006; 29:1420-1432.
15
16.Martin Gallan' P, Carrascosa A, Gussinye' M, Dominguez C. Biomarkers of diabetes-associated oxidative stress and antioxidant status in young diabetic patients with or without subclinical complications. Free Radic Biol Med 2003;34:1563-1574.
16
17.Breuer W, Hershko C, Cabantchik ZI. The importance of nontransferrin bound iron in disorders of iron metabolism. Transfus Sci 2000; 23:185-192.
17
18.Van Campenhout A,Van Campenhout CM, Lagrou AR, Manuel-y-Keenoy B. Transferrin modifications and lipid peroxidation: implications in diabetes mellitus. Free Radic Res 2003; 37:1069-1077.
18
19.Gallou G, Ruelland A, Campion L, Maugendre D, Le Moullec N, Legras B, et al. Increase in thiobarbituric acid-reactive substances and vascular complications in type 2 diabetes mellitus. Diabete Metab 1994; 20:258¬264.
19
20.Koga T, Keiko M, Terao J. Protective effet of vitamin E analog, phosphatidylchromanol, against oxidative hemolysis of human erythrocytes. Lipids 1980; 33:589-595.
20
21.Valkonen M, Kuusi T. Spectrophotometer assay for total peroxyl radical-trapping antioxidant potential in human serum. J Lipid Res 1997; 38:823-833.
21
22.Sen S, Kar M, Roy A, Chakraborti AS. Effect of nonenzymatic glycation on function and structural properties of hemoglobin. Biophys Chem 2005; 113:289-298.
22
23.Fujimoto S, Kawakami N, Ohara A. Nonenzymatic glycation of transferri: decrease of iron-binding capacity and increase of oxygen radical production. Biol Pharm Bull 1995; 18:396-400.
23
24.Van Campenhout A, Van Campenhout C, Lagrou AR, Manuel-y-Keenoy B. Effect of in vitro glycastion on Fe3+ binding and Fe3+ isoforms of transferrin. Clin Chem 2004; 50: 1640-1649.
24
25.Van Campenhout A, Van Campenhout C, Olyslager YS, Van Damme O, Lagrou AR, Manuel-y-Keenoy B. A novel method to quantify in vivo transferrin glycation: application in diabetes mellitus. Clin Chim Acta 2006; 370:115-123.
25
ORIGINAL_ARTICLE
Effects of Administration of Perinatal Bupropion on the Population Spike Amplitude in Neonatal Rat Hippocampal Slices
Objective(s)
Bupropion is an atypical antidepressant that is widely used in smoke cessation under FDA approval. The study of synaptic effects of bupropion can help to finding out its mechanism(s) for stopping nicotine dependence. In this study the effects of perinatal bupropion on the population spike (PS) amplitude of neonates were investigated.
Materials and Methods
Hippocampal slices were prepared from 18-25 days old rat pups. The experimental groups included control and bupropion-treated. Bupropion (40 mg/Kg, i.p.) was applied daily in perinatal period as pre-treatment. Due to the studying acute effects, bupropion was also added to the perfusion medium (10, 50, 200 pM for 30 min). The evoked PS was recorded from pyramidal layer of CA1 area, following stimulation of Schaffer collaterals. Results
A concentration of 10 pM bupropion had no significant effects on the PS amplitude. The 50 pM concentration of bupropion reduced the amplitude of responses in 50% of the studied cases. At a concentration of 200 pM, the recorded PS amplitudes were reduced in all slices (n= 22). Amplitude was completely abolished in 8 out of the 22 slices. The decrease of the PS amplitude was found to be more in the non-pre-treated slices than in the pre-treated slices when both were perfused with 200 pM bupropion.
Conclusion
The results showed the perinatal exposure to bupropion and its acute effects while indicating that at concentrations of 50 and 200 pM bupropion reduced the PS amplitude. It was also found that there was evidence of synaptic adaptation in comparison of bupropion-treated and non-treated slices whereas they were both perfused with 200 pM.
https://ijbms.mums.ac.ir/article_5114_278ae9bdfa30bba029cab0a9865ae7f5.pdf
2010-10-01
200
206
10.22038/ijbms.2010.5114
Bupropion
Hippocampus
Population Spike
Rat
Slice
Soomaayeh
Heysieat-talab
1
Department of Biology, Faculty of Science, Urmia University, Urmia, Iran
AUTHOR
Samad
Zare
s-zare@urmia.ac.ir
2
Department of Biology, Faculty of Science, Urmia University, Urmia, Iran
AUTHOR
Firouz
Ghaderi Pakdel
info@fgpakdel.com
3
Department of Physiology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran
LEAD_AUTHOR
Mina
Mokhtari hashtjin
4
Department of Biology, Faculty of Science, Urmia University, Urmia, Iran
AUTHOR
1.Hayford KE, Patten CA, Rummans TA, Schroeder DR, Offord KP, Croghan IT, et al. Efficacy of bupropion for smoking cessation in smokers with a former history of major depression or alcoholism. Br J Psychiatry 1999; 174:173-178.
1
2.Balfour DJ. The pharmacology underlying pharmacotherapy for tobacco dependence: a focus on bupropion. Int J Clin Pract 2001; 55:53-57.
2
3. Ascher JA, Cole JO, Colin JN, Feighner JP, Ferris RM, Fibiger HC, et al. Bupropion: a review of its mechanism of antidepressant activity. J Clin Psychiatry 1995; 56:395-401.
3
4.Dwoskin LP, Rauhut AS, King- Pospisil KA, Bardo MT. Review of the pharmacology and clinical profile of Bupropion, an antidepressant and tobacco use cessation agent. CNS Drug Rev 2006; 12:178-207.
4
5.Ferris RM, Beaman OJ. Bupropion: a new antidepressant drug, the mechanism of action of which is not associated with down-regulation of postsynaptic beta-adrenergic, serotonergic (5-HT2), alpha 2-adrenergic, imipramine and dopaminergic receptors in brain. Neuropharmacology 1983; 22:1257-1267.
5
6.Dong J, Blier P. Modification of norepinephrine and serotonin, but not dopamine, neuron firing by sustained bupropion treatment. Psychopharmacology 2001; 155:52-57.
6
7.ElMansari M, Ghanbari R, Janssen S, Blier P. Sustained administration of bupropion alters the neuronal activity of serotonin, norepinephrine but not dopamine neurons in the rat brain. Neuropharmacolology 2008; 55:1191-1198.
7
8.Li SX, Perry KW, Wong DT. Influence of fluoxetine on the ability of bupropion to modulate extracellular dopamine and norepinephrine concentrations in three mesocorticolimbic areas of rats. Neuropharmacology 2002; 42:181-190.
8
9.Mansvelder HD, Fagen ZM, Chang B, Mitchum R, Mc Gehee DS. Bupropion inhibits the cellular effects of nicotine in the ventral tegmental area. Biochem Pharmacol 2007; 74:1283-1291.
9
10.Placzek AN, Zhang TA, Dani JA. Nicotinic mechanisms influencing synaptic plasticity in the hippocampus. Acta Pharmacol Sin 2009; 30:752-760.
10
11.Kauer JA. Learning mechanisms in addiction: synaptic plasticity in the ventral tegmental area as a result of exposure to drugs of abuse. Annu Rev Physiol 2004; 66:447-475.
11
12.Garrett BE, Rose CA, Henningfield JE. Tobacco addiction and pharmacological interventions. Expert Opin Pharmacolther 2001; 2:1545-1555.
12
13.Dani JA, De Biasi M. Synaptic plasticity and nicotine addiction. Neuron 2001; 31:349-352.
13
14.Jones S, Bonci A. Synaptic plasticity and drug addiction. Curr Opin Pharmacol 2005; 5:20-25.
14
15.Gould TJ. Nicotine and hippocampus- dependent learning. Mol Neurobiol 2006; 34:93-107.
15
16.Kenney JW, Gould TJ. Modulation of hippocampus-dependent learning and synaptic plasticity by nicotine. Mol Neurobiol 2008; 38:101- 121.
16
17.Watanabe Y, Saito H, Abe K. Tricyclic antidepressants block NMDA receptor-mediated synaptic responses and induction of long term potentiation in rat hippocampal slices. Neuropharmacology 1993; 32:479- 486.
17
18.Stewart CA, Reid IC. Repeated ECS and fluoxetine administration have equivalent effects on hippocampal synaptic plasticity. Psychopharmacology 2000; 148:217-223.
18
19.Birnstiel S, Haas HL. Acute effects of antidepressant drugs on long-term potentiation (LTP) in rat Hippocampal slices. Naunyn-Schmiedebergs Arch Pharmacol 1991; 344:79-83.
19
20.Crawley JN, Gerfen CR, Rogawski MA, Sibley DR, Skolnick P, Wray S. Synaptic plasticity in the hippocampal slice preparation. In: Taylor GP. editors. Current protocols in neurosci John Wiley & Sons, Inc.; 2003.
20
21.Wang T, Kass IS. Preparation of brain slices. In: Rayne RC. editor. Methods in molecular biology Totowa: Humana Press Inc; 1997.p.1-14.
21
22.Massicotte G, Bernard J,Ohayon M. Chronic effects of trimipramine, an antidepressant, on hippocampal synaptic plasticity. Behav Neural Biol 1993; 59:100-106.
22
23.Langosch JM, Walden J. Affects of the atypical antidepressant trimipramine on neuronal excitability and long¬term potentiation in guinea pig hippocampal slices. Progress in Neuro- Psychopharmacol Biological Psychia 2002; 26:299-302.
23
24.Stewart CA, Reid IC. Antidepressant mechanisms: functional and molecular correlates of excitatory amino acid neurotransmission. Mol Psychiatry 2002; 7:15-22.
24
25.D’Sa C, Duman RS. Antidepressants and neuroplasticity. Bipolar Disord 2002; 4:183-194.
25
26.Duman RS, Malberg J, Thome J. Neural plasticity to stress and antidepressant treatment. Biol Psychiatry 1999; 46:1181-1191.
26
27.Castren E. Neurotrophic effects of antidepressant drugs. Curr Opin Pharmacol 2004; 4:58-64.
27
28.Zahorodna A, Bijak M. An antidepressant induced decrease in the responsiveness of Hippocampal neurons to group I metabotropic glutamate receptor activation. Eur J Pharmacol 1999; 386:173-179.
28
29.Yashiro K, Philpot BD. Regulation of NMDA receptor subunit expression and its implications for LTD, LTP, and metaplasticity. Neuropharmacology 2008; 55:1081-1094.
29
30.Bobula B, Tokarski K, Hess G. Repeated administration of antidepressants decreases field potentials in rat frontal cortex. Neuroscience 2003; 120:765-769.
30
31.Popoli M, Gennarelli M, Racagni G. Modulation of synaptic plasticity by stress and antidepressants. Bipolar Disord 2002; 4: 166-182.
31
32.Reid IC, Stewart CA. Brain plasticity and antidepressant treatments: new cells, new connections. Neurotox Res 2004; 6:483-491.
32
33.Mc Bain CJ, Freund TF, Mody I. Glutamatergic synapses on to Hippocampal interneuron: precision timing without lasting plasticity. Trends Neurosci 1999; 22:228-235.
33
34.Baskys A, Wang S, Remington G, Wotjtowicz JM. Haloperidol and loxapine but not clozapine increase synaptic responses in the hippocampus. Eur J Pharmacol 1993; 235:305-307.
34
35.Chen Long, Charles R Yang. Interaction of dopamine D1 and NMDA receptors mediates acute clozapine potentiation of glutamate EPSPs in rat prefrontal cortex. J Neurophysiol 2002; 87:2324-2336.
35
ORIGINAL_ARTICLE
The Effects of Cholestasis and Cirrhosis on Gastric Acid and Pepsin Secretions in Rat: Involvement of Nitric Oxide
Objective(s)
The liver has major role in the organism homeostasis, interactions with other systems, synthesis and metabolism of bile production, drug detoxification and hormone inactivation. Cholestasis can be defined as an impairment of the bile flow which can lead to hepatocytes necrosis and finally cirrhosis. Some studies reported a gastric acid secretion reduction in cirrhotic subjects, while others reported normal production gastric acid secretion. Our aim was to evaluate the effects of cholestasis and cirrhosis on gastric acid and pepsin secretions and its possible mechanism in rat.
Materials and Methods
Male Wistar rats were randomly divided into five groups (n= 8): control, cholestasis, sham cholestasis, cirrhosis and sham cirrhosis. Laparatomy was done under general anesthesia and then bile duct ligation (BDL) was performed. After 2 and 4 weeks in cholestasis and cirrhosis groups respectively, gastric content was collected by wash-out technique. Basal and stimulated acid and pepsin secretions were measured by using titration and the Anson method respectively in all groups. In order to measure stimulated acid and pepsin secretions, pentagastrin (25 pg/kg, i.p.) was used. Nitric Oxide (NO) metabolites of gastric tissue were determined by Griess microassy method.
Results
Acid and pepsin secretions were significantly reduced in cholestatic and cirrhotic rats in comparison with control and sham groups (P< 0.01). NO metabolite of gastric tissue was significantly increased in cholestatic and cirrhotic rats (P< 0.01).
Conclusion
Reducing of gastric acid and pepsin output in cholestatic and cirrhotic rats may be due to increasing in NO content of gastric tissue.
https://ijbms.mums.ac.ir/article_5115_b51998898a9c1aca7a928c1ea1567a05.pdf
2010-10-01
207
212
10.22038/ijbms.2010.5115
cholestasis
Gastric acid
Liver Cirrhosis
Nitric oxide
Pepsin
Fatemeh
Nabavizadeh
nabavizadeh2000@yahoo.com
1
Department of Physiology, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Rohallah
Moloudi
2
Department of Physiology, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Ahmad Reza
Dehpour
dehpoura@sina.tums.ac.ir
3
Department of Physiology, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Hossein
Nahrevanian
mobcghn@gmail.com
4
Pasteur Institute of Iran, Tehran, Iran
AUTHOR
Kaveh
Shahvaisi
5
Department of Physiology, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Ehsan
Salimi
6
Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
1.Gaskari SA, Honar H, Lee SS. Therapy insight: cirrhotic cardiomyopathy. Nat Clin Pract Gastroenterol Hepatol 2006; 3:329-337.
1
2.Paumgartner G. Medical treatment of cholestatic liver diseases: From pathobiology to pharmacological targets. World J Gastroenterol 2006; 12:4445-4451.
2
3.Paumgartner G, Beuers U. Ursodeoxycholic acid in cholestatic liver disease: mechanisms of action and therapeutic use revisited. Hepatology 2002; 36:525-531.
3
4.Wong F. Cirrhotic cardiomyopathy. Hepatol Int 2009; 3:294-304.
4
5.Avila FT, Avila FS, de-Sicilia MS, Chavez-Tapia NC, et al. Prevalence of metabolic syndrome, obesity and diabetes type 2 in cryptogenic cirrhosis. World J Gastroenterol 2008; 14:4771-4775.
5
6.Mesejo A, Juan YM, Serrano A. Liver cirrhosis and encephalopathy: Clinical and metabolic consequences and nutritional support. Nutr Hosp 2008; 23:8-18.
6
7.Castilla-Cortazar I, Pascual M, Urdaneta E, Pardo J, Puche JE, Vivas B, et al. Jejunal microvilli atrophy and reduced nutrient transport in rats with advanced liver cirrhosis: improvement by Insulin-like Growth Factor I. BMC Gastroenterol 2004; 4:12.
7
8.Conchillo M, Prieto J, Quiroga J. Insulin-like growth factor I (IGF-I) and liver cirrhosis. Rev Esp Enferm Dig (Madrid) 2007; 99:156-164.
8
9.Wang X, Zhong YX, Zhang ZY, Lu J, Lan M, Miao JY, Guo XG, Shi YQ, Zhao YQ, Ding J, Wu KC, Pan BR, Fan DM. et al. Effect of L-NAME on nitric oxide and gastrointestinal motility alterations in cirrhotic rats. World J Gastroenterol 2002; 8:328-332.
9
10.Schiedermaier P, Harrison P, Arthur M, Grandt D, Sutton R, Drewe J, et al. Effect of the Somatostatin Analogue Lanreotide on Meal-Stimulated Portal Blood Flow in Patients with Liver Cirrhosis. Digestion 2002; 65:56-60.
10
11.Konturek SJ, Gonciarz M, Bielanski W, Mazur W, Mularczyk A, Konturek PC, et al. Progastrin and its products from patients with chronic viral hepatitis and liver cirrhosis. Scand J Gastroenterol 2003; 38:643-647.
11
12.Lodato F, Azzaroli F, Di Girolamo M, Feletti V, Cecinato P, Lisotti A, et al .Proton pump inhibitors in cirrhosis: Tradition or evidence based practice? World J Gastroenterol 2008; 14:2980-2985.
12
13.Konturek SJ, Gonciarz M, Gonciarz Z, Bielanski W, Mazur W, Mularczyk A, et al. Progastrin and its products from patients with chronic viral hepatitis and liver cirrhosis . Scand J Gastroenterol 2003; 38:643-647.
13
14.Kitano S, Dolgor B .Does portal hypertension contribute to the pathogenesis of gastric ulcer associated with liver cirrhosis? J Gastroenterol 2000; 35:79-86.
14
15.Cortez-pinto H, Ferra MA, Baptista A, Demoura MC, De Moura MC, Portela-Gomes GM l. Serum gastrin and gastrin=immunoreactive cells in the antral mucosa of patients with alcoholic liver disease. APMIS 2000; 108: 51-56.
15
16.Yeh JL , Peng YC , Tung CF , Chen GH , Chow WK, Chang CS, et al. Role of Helicobacter pylori in cirrhotic patients with dyspepsia: A13C-urea breathe test study. Adv Ther 2001; 18:140-150.
16
17.Nahavandi A, Dehpour AR, Mani AR, Homayounfar H, Abdoli A, Abdolhoseini MR, et al. The role of nitric oxide in bradycardia of rats with obstructive cholestasis . Eur J Pharmacol 2001; 411: 135-141.
17
18.Nabavizadeh F , Zahedi Asl S , Garib Naseri MK, Vahedian J. Effects of thyroid hormones on basal and stimulated gastric acid secretion due to histamine, carbachol and pentagastrin in rats. Saudi Med J 2003; 24:341-346.
18
19.Nabavizadeh F, Salimi E, Sadroleslami Z, Vahedian J. Saffron (Crocus sativus) increases gastric acid and pepsin secretions in rats: Role of nitric oxide (NO). Afr J Pharmacy Pharmacol 2009; 3:181-184.
19
20.Nahrevanian H, Gholizadeh J, Farahmand M, Assmar M, Sharifi K, Ayatollahi Mousavi SA, et al. Nitric oxide induction as a novel immunoepidemiological target in malaria-infected patients from endemic areas of the Islamic Republic of Iran. Scand J Clin Lab Invest 2006; 66:201-209.
20
21.Zullo A, Romiti A, Rinaldi V, Vecchione A, Hassan C, Winn S, et al. Gastric epithelial cell proliferation in patients with liver cirrhosis. Dig Dis Sci 2001; 46:550-554 .
21
22. Celinski K, Konturek PC, Slomka M, Cichoz-Lach H, Gonciarz M, Bielanski W, et al. Altered basal and postprandial plasma melatonin, gastrin, ghrelin, leptin and insulin in patients with liver cirrhosis and portal hypertension without and with oral administration of melatonin or tryptophan. J Res 2009; 46:408-414.
22
23. Izbeki F,Kiss I, Wittmann T, Varkonyi T, Varkonyi TT, Legrady P, et al.Impaired accommodation of proximal stomach in patients with alcoholic liver cirrhosis. Scand J Gastroenterol 2002; 37: 1403-1410.
23
24.Nam YJ, Kim SJ, Shin WC, Lee JH, Choi WC, Kim KY, Han TH.. Gastric pH and Helicobacter pylori Infection in Patients with Liver Cirrhosis. Korean J Hepatol 2004; 10:216-222.
24
25.Kamalaporn P, Sobhonslidsuk A, Jatchavala J, Atisook K, Rattanasiri S, Pramoolsinsap Cl. Factors predisposing to peptic ulcer disease in asymptomatic cirrhotic patients. Aliment Pharmacol Ther 2005; 21:1459-1465.
25
26.Konturek SJ, Gonciarz M, Gonciarz Z, Bielanski W, Mazur W, Mularczyk A, et al. Progastrin and its products from patients with chronic viral hepatitis and liver cirrhosis. Scand J Gastroenterol 2003; 38:643-647.
26
27.Dijkstra G, Van GH, Jansen PL, Moshage Hl. Targeting nitric oxide in the gastrointestinal tract. Curr Opin Investig Drugs 2004; 5:529-536.
27
28.Berg A, Kechagias S, Sjostrand SE, Ericson AC. Morphological Support for Paracrine Inhibition of Gastric Acid Secretion by Nitric Oxide in Humans. Scand J Gastroenterol 2001; 36: 1016-1021.
28
29. Holm M, Powell T, Casselbrant A, Johansson B, Fa'ndriks L. Dynamic involvement of the inducible type of nitric oxide synthase in acid-induced duodenal mucosal alkaline secretion in the rat. Dig Dis Sci 2001; 46:1765-1771.
29
30.Nylander O, Ha'llgren A, Sababi M. COX inhibition excites enteric nerves that affect motility, alkaline secretion, and permeability in rat duodenum. Am J Physiol Gastrointest Liver Physiol 2001; 281:1169-1178.
30
31.Hasebe K, Horie S, Komasaka M, Yano S, Watanabe K. Stimulatory effects of nitric oxide donors on gastric acid secretion in isolated mouse stomach. Eur J Pharmacol 2001; 420:159-164.
31
32.Hasebe K, Horie S, Noji T, Watanabe K, Yano S. Stimulatory effects of endogenous and exogenous nitric oxide on gastric acid secretion in anesthetized rats. Nitric Oxide 2005; 13:264-271.
32
ORIGINAL_ARTICLE
Hepatitis B Virus Surface Antigen Variants Clustered Within Immune Epitopes in Chronic Hepatitis B Carriers from Hormozgan Province, South of Iran
Objective(s)
The aim of this study was to characterize the hepatitis B virus surface protein genotypes and sequence variations among hepatitis B virus surface antigen (HBsAg) positive chronic patients in Hormozgan province, south of Iran.
Materials and Methods
A total of 8 patients enrolled in this study. The surface gene was amplified and directly sequenced. Genotypes and nucleotide/amino acid substitutions were identified compared to the sequences obtained from the database.
Results
All strains belonged to genotype D. Overall 77 “mutations” occurred at 45 nucleotide positions, of them, 44 (57.14%) were silent (no amino acid altering) and 33 (42.86%) were missense (amino acid changing). A number of 24 (80%) out of 30 amino acid changes occurred in different immune epitopes within surface protein, of which, 9 (30%) in B cell epitopes in 7 residues (2 occurred in “a” determinant region); 8 (42.1%) in T helper epitopes in 7 residues and 7 (10%) in 4 residues inside CTL epitopes.
Conclusion
Hepatitis B virus genome containing mutated immune epitopes no longer could be recognized by specific T- cells of the host immune surveillance and did not enhance anti-HBs production. This could led to the progression of chronicity of hepatitis B virus infection.
https://ijbms.mums.ac.ir/article_5117_b25fcd4e69623b11f260d3625f13b98b.pdf
2010-10-01
213
224
10.22038/ijbms.2010.5117
HBV genotypes
HBV genotype D
HBV genotype in Iran
HBV immune epitopes
Mehdi
Norouzi
mnorouzi@tums.ac.ir
1
Iranian National Institute for Genetic Engineering and Biotechnology, Tehran, Iran
AUTHOR
Seyed Ali
Ghorashi
2
Iranian National Institute for Genetic Engineering and Biotechnology, Tehran, Iran
AUTHOR
Behrooz
Ataei
3
Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Majid
Yaran
4
Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Reza
Malekzadeh
malekzadeh@gmail.com
5
Digestive Disease Research Center, Shariati Hospital, Tehran, Iran
AUTHOR
Seyed Moayyed
Alavian
6
Baqiyatallah University of Medical Sciences, Baqiyatallah Research Centre for Gastroenterology and Liver Disease, Tehran, Iran
AUTHOR
Mohammad Ali
Judaki
7
Hepatitis B Molecular Laboratory,Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Shiva
Ghamari
8
Hepatitis B Molecular Laboratory,Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Alireza
Namazi
9
Hepatitis B Molecular Laboratory,Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Ramin
Rahimnia
10
Hepatitis B Molecular Laboratory,Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Abolfazl
Khedive
11
Hepatitis B Molecular Laboratory,Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Seyed Mohammad
Jazayeri
eve.holly@gmail.com
12
Hepatitis B Molecular Laboratory,Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
1.Wallace LA, Carman WF. Surface gene variation of HBV: Scientific and medical relevance. J Viral Hepatitis 1997; 3:5-16.
1
2.Honorati MC, Dolzani P, Mariani E, Piacentini A, Lisignoli G, Ferrari C, Facchini A. Epitope specificity of Th0/Th2 CD4+ T-lymphocyte clones induced by vaccination with rHBsAg vaccine. Gastroenterology 1997; 112:2017-2027.
2
3.Mancini-Bourgine M, Fontaine H, Brechot C, Pol S, Michel ML. Immunogenicity of a hepatitis B DNA vaccine administered to chronic HBV carriers. Vaccine 2006; 24:4482-4489.
3
4.Ducos J Bianchi, Mondain AM, Pageaux G, Conge AM, Poncet R, Vendrell JP, et al. Hepatitis B virus (HBV)specific in vitro antibody production by peripheral blood mononuclear cells (PBMC) after vaccination by recombinant hepatitis B surface antigen (rHBsAg). Clin Exp Immunol 1996; 103:15-18.
4
5.Barnaba V, Franco A, Paroli M, Benvenuto R, De Petrillo G, Burgio VL. Selective expansion of cytotoxic T lymphocytes with a CD4+CD56+surface phenotype and a T helper type 1 profile of cytokine secretion in the liver of patients chronically infected with hepatitis B virus. J Immunol 1994; 152:3074-3087.
5
6.Norder H, Hammas B, Lofdahl S, Courouce AM, Magnius LO. Comparison of the amino acid sequences of nine different serotypes of hepatitis B surface antigen and genomic classification of the corresponding hepatitis B virus strains. J Gen Virol 1992; 73:1201-12018.
6
7.Norder H, Courouce AM, Magnius LO. Molecular basis of hepatitis B virus serotype variations within the four major subtypes. J Gen Virol 1992; 73:3141-3145.
7
8.Chisari FV. Immunobiology and pathogenesis of viral hepatitis. Edizioni Minerva Medica, Turin. 1997.
8
9.Mesenas SJ, Chow WC, Zhao Y, Lim GK, Oon CJ, Ng HS. Wild-type and 'a' epitope variants in chronic hepatitis B virus carriers positive for hepatitis B surface antigen and antibody. J Gastroenterol Hepatol 2002; 17:148-152.
9
10.Friedt M, Gerner P, Wintermeyer P, Wirth S. Complete hepatitis B virus genome analysis in HBsAg positive mothers and their infants with fulminant hepatitis B. BMC Gastroenterol 2004; 4:11.
10
11.Ozaslan M, Ozaslan E, Barsgan A, Koruk MJ. Mutations in the S gene region of hepatitis B virus genotype D in Turkish patients. J Genet 2007; 86:195-201.
11
12.Tabor E. Infections by hepatitis B surface antigen gene mutants in Europe and North America. J Med Virol 2006; 78:S43-47.
12
13. Song BC, Kim SH, Kim H, Ying YH, Kim HJ, Kim YJ, et al. Prevalence of naturally occurring surface antigen variants of hepatitis B virus in Korean patients infected chronically. J Med Virol 2005; 76:194-202.
13
14.Bahramali G, Sadeghizadeh M, Amini-Bavil-Olyaee S, Alavian SM, Behzad-Behbahani A, Adeli A, et al. Clinical, virologic and phylogenetic features of hepatitis B infection in Iranian patients. World J Gastroenterol 2008; 14:5448-5453.
14
15.Ireland JH, O'Donnell B, Basuni AA, Kean JD, Wallace LA, Lau GK, et al. Reactivity of 13 in vitro expressed hepatitis B surface antigen variants in 7 commercial diagnostic assays. Hepatology 2000; 31:1176-1182.
15
16.Weber B. Genetic variability of the S gene of hepatitis B virus: clinical and diagnostic impact. J Clin Virol 2005; 32:102-112.
16
17.Weber B. Diagnostic impact of the genetic variability of the hepatitis B virus surface antigen gene. J Med Virol 2006; 78:S59-65.
17
18.Hollinger FB. Hepatitis B virus genetic diversity and its impact on diagnostic assays. J Viral Hepat 2007; 1:11-5.
18
19.Pourkarim MR, Amini-Bavil-Olyaee S, Verbeeck J, Lemey P, Zeller M, Rahman M, et al. Molecular evolutionary analysis and mutational pattern of full-length genomes of hepatitis B virus isolated from Belgian patients with different clinical manifestations. J Med Virol 2010; 82:379-389.
19
20.Datta S, Panigrahi R, Biswas A, Chandra PK, Banerjee A, Mahapatra PK, et al. Genetic characterization of hepatitis B virus in peripheral blood leukocytes: evidence for selection and compartmentalization of viral variants with the immune escape G145R mutation.J Virol 2009; 83:9983-9992.
20
21.Sloan RD, Strang AL, Ramsay ME, Teo CG. Genotyping of acute HBV isolates from England, 1997-2001. J Clin Virol 2009; 44:157-160.
21
22.Salazar M, Deulofeut H, Granja C, Deulofeut R, Yunis DE, Marcus-Bagley D, et al. Normal HBsAG presentation and T-cell defect in the immune response of nonresponders. Immunogenetics 1995; 41:366-374.
22
23.Bauer T, Weinberger K, Jilg W. Variants of two major T cell epitopes within the hepatitis B surface antigen are not recognized by specific T helper cells of vaccinated individuals . Hepatology 2002; 455-465.
23
24.Jazayeri and Carman. Virus escape, CTL or B cell epitopes Hepatitis Monthly 2005; 5:133-136.
24
25.Chen M, Salberg M, Thung SN, Hughes J, Jones J, Milich DR. Modelling the T helper cell response in acute and chronic hepatitis B virus infection using T-cell receptor transgenic mice. Antiviral Res 2001; 52:99-111.
25
26.Liu CJ, Kao JH, Shau WY, Chen PJ, Lai MY, Chen DS. Naturally occurring hepatitis B surface gene variants in chronic hepatitis B virus infection: correlation with viral serotypes and clinical stages of liver disease. J Med Virol 2002; 68:50-59.
26
27.Barnaba V, Franco A, Alberti A, Balsano C, Benvenuto R, Balsano F. Recognition of hepatitis B virus envelope proteins by liver-infiltrating T lymphocytes in chronic HBV. Infection. J immunol 1989; 143:2650-2655.
27
28.Khakoo SI, Ling R, Scott I, Dodi AI, Harrison TJ, Dusheiko GM, et al. Cytotoxic T lymphocyte responses and CTL epitope escape mutation in HBsAg, anti-HBe positive individuals. Gut 2000; 4: 256.
28
29.Yamauchi K, Nakamura T, Yonemitsu H, Sekiya H, Katoh J, Obata H. Possible role of preS2 peptides presented by MHC class I antigen in the pathogenesis of chronic hepatitis B. J Hepatol 1993; 17:S6-9.
29
30.Carman WF, Thursz M, Hadziyannis S, McIntyre G, Colman K, Gioustoz A, et al. Hepatitis B e antigen negative chronic active hepatitis: hepatitis B virus core mutations occur predominantly in known antigenic determinants. J Viral Hepat 1995; 2:77-84.
30
31.Carman WF, Boner W, Fattovich G, Colman K, Dornan ES, Thursz M, et al. Hepatitis B virus core protein mutations are concentrated in B cell epitopes in progressive disease and in T helper cell epitopes during clinical remission. J Infect Dis 1997; 175:1093-10100.
31
32.Hosono S, Tai PC, Wang W, Ambrose M, Hwang DG, Yuan TT, et al. Core antigen mutations of human hepatitis B virus in hepatomas accumulate in MHC class II-restricted T cell epitopes. Virology 1995; 212:151-162.
32
33.Rehermann B, Pasquinelli C, Mosier SM, Chisari FV. Hepatitis B virus (HBV) sequence variation of cytotoxic T lymphocyte epitopes is not common in patients with chronic HBV infection. J Clin Invest 1995;
33
34.Maruyama T, Kuwata S, Koike K, Iino S, Yasuda K, Yotsuyanagi H, et al. Precore wild-type DNA and immune complexes persist in chronic hepatitis B after seroconversion: no association between genome conversion and seroconversion. Hepatology 1998; 27:245-53.
34
35.Jazayeri SM, Dornan E, Boner W, Waketing M, Hadziyannis S, Fattovich G, et al. Distribution of in vitro expressed HBV core protein from isolates is dependent upon sequence and correlates with disease pattern. J Infect Dis 2004; 189:1634-1645.
35
ORIGINAL_ARTICLE
Synthesis and Effects of 4,5-Diaryl-2-(2-alkylthio-5-imidazolyl) Imidazoles as Selective Cyclooxygenase Inhibitors
Objective(s)
In recent years highly selective COX-2inhibitors were withdrawn from the market because of an increased risk of cardiovascular complications. In this study we were looking for potent compounds with moderate selectivity for cox-2. So, four analogues of 4, 5-diaryl-2-(2-alkylthio-5-imidazolyl) imidazole derivatives were synthesized and their anti-inflammatory and anti-nociceptive activities were evaluated on male BALB/c mice (25-30 g). Molecular modeling and in vitro COX-1 and COX-2 isozyme inhibition studies were also performed.
Materials and Methods
2-(2-Alkylthio-5-imidazolyl)-4,5-diphenylimidazole compounds were obtained by the reaction of benzyl with 2-alkylthio-1-benzylimidazole-5-carbaldehyde, in the presence of ammonium acetate. Spectroscopic data and elemental analysis of compounds were obtained and their structures elucidated. Anti-nociception effects were examined using writhing test in mice. The effect of the analogues (7.5, 30, 52.5 and 75 mg/kg) against acute inflammation were studied using xylene-induced ear edema test in mice. Celecoxib (75 mg/kg) was used as positive control.
Results
All four analogues exhibited anti-nociceptive activity against acetic acid induced writhing, but did not show significant analgesic effect (P< 0.05) compared with celecoxib. It was shown that analogues injected 30 min before xylene application reduced the weight of edematic ears. All analogues were found to have less selectivity for COX-2 in comparison to celecoxib.
Conclusion
Injected doses of synthesised analogues possesses favorite anti-nociceptive effect and also has antiinflammatory effects, but comparing with celecoxib this effect is not significantly different. On the other hand selectivity index for analogues is less than celecoxib and so we expect less cardiovascular side effects for these compounds.
https://ijbms.mums.ac.ir/article_5121_35819551973c5da48eb63519c74df4e3.pdf
2010-10-01
225
231
10.22038/ijbms.2010.5121
Analgesic
Anti-inflammatory
Imidazoles
Mohammad Reza
Saberi
1
School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Farzin
Hadizadeh
hadizadehf@mums.ac.ir.
2
Biotechnology Research Center, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad , Iran
LEAD_AUTHOR
Mohsen
Imenshahidi
3
School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Hadi
Shakeri
4
Biotechnology Research Center, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad , Iran
AUTHOR
Seyedeh Toktam
Ziaee
5
Biotechnology Research Center, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad , Iran
AUTHOR
Mohammad Ali
Ghafuri
6
School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Ramin
Sakhtianchi
7
School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Zohreh
Badieyan
8
School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Somieh
Hajian
9
School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
1.Fu JY, Masferrer JL, Seibert K, Raz A, Needleman P. The induction and suppression of prostaglandin H2 synthase (cyclooxygenase) in human monocytes. J Biol Chem 1990; 265:16737-16740.
1
2.Xie WL, Chipman JG, Robertson DL, Erikson RL, Simmons DL. Expression of a mitogen-responsive gene encoding prostaglandin synthase is regulated by mRNA splicing. Proc Natl Acad Sci USA 1991; 88:2692-2696.
2
3.Smith WL, Dewitt DL. Prostaglandin endoperoxide H synthases-1 and -2. Adv Immunol 1996; 62:167-215.
3
4.Herschman HR. Prostaglandin synthase 2. Biochim Biophys Acta 1996; 1299:125-140.
4
5.Kawamori T, Rao CV, Seibert K, Reddy BS. Chemopreventive activity of celecoxib,a specific cyclooxygenase-2 inhibitor, against colon carcinogenesis. Cancer Res 1998; 58:409-412.
5
6.Katori M, Majima M. Cyclooxygenase-2: Its rich diversity of roles and possible application of its selective inhibitors. Inflamm Res 2000; 49:367-392.
6
7.Vane JR, Botting RM. Anti-inflammatory drugs and their mechanism of action. Inflamm Res 1998; 47:S78-87.
7
8.Bing RJ, Lomnicka M. Why do cyclo-oxygenase-2 inhibitors cause cardiovascular events? J Am Coll Cardiol 2002; 39:521-522.
8
9.Chen C-S, Tan C-M, Huang C-H, Chang L-C, Wang J-P, Cheng F-C, et al. Discovery of 3-(4-bromophenyl)- 6-nitrobenzo[1.3.2]dithiazolium ylide 1,1-dioxide as a novel dual cyclooxygenase/5-lipoxygenase inhibitor that also inhibits tumor necrosis factor-[alpha] production. Bioorg Med Chem 2010; 8:597-604.
9
10.Penning TD, Talley JJ, Bertenshaw SR, Carter JS, Collins PW, Docter S. Synthesis and biological evaluation of the 1.5 diarylpyrazole class of cyclooxygenase-2 inhibitors: identification of 4-[5-(4-methylphenyl)-3-(trifluoromethyl)- 1H-pyrazol-1-yl]benze nesulfonamide (SC-58635, celecoxib). J Med Chem 1997; 40:1347-1365.
10
11.Prasit P, Wang Z, Brideau C, Chan CC, Charleson S, Cromlish W, et al.The discovery of rofecoxib, [MK 966, VIOXX®, 4-(4'-methylsulfonylphenyl)-3-phenyl-2(5H)-furanone],an orally active cyclooxygenase-2 inhibitor. Bioorg Med Chem Lett 1999; 9:1773-1778.
11
12.Friesen RW, Dube D, Fortin R, Frenette R, Prescott S, Cromlish W, et al. Novel 1,2-diarylcyclobutenes: Selective and orally active COX-2inhibitors. Bioorg Med Chem Lett 1996; 6:2677-2682.
12
13.Talley JJ, Brown DL, Carter JS, Graneto MJ, Koboldt CM, Masferrer JL, et al. 4-[5-Methyl-3-phenylisoxazol-4-yl]- benzenesulfonamide, valdecoxib: a potent and selective inhibitor of COX-2. J Med Chem 2000; 43:775-777.
13
14.Zarghi A, Rao PN, Knaus EE. Design and synthesis of new rofecoxib analogs as selective cyclooxygenase-2 (COX-2) inhibitors: replacement of the methanesulfonyl pharmacophore by a N-acetylsulfonamido bioisostere. J Pharm Pharm Sci 2007; 10:159-167.
14
15.Isikdag I, Meric A. Syntheses and analgesic activities of some 2-substituted-4,5-diphenyl and 1,2-disubstituted 4.5-diphenyl imidazole derivatives. Boll Chim Farm 1999; 138:24-29.
15
16.Hadizadeh F, Vosooghi R. Synthesis of a-[5-(5-Amino-1,3,4-thiadiazol-2-yl)-2-imidazolylthio]acetic acids. J Heterocyclic Chem 2008; 45:1477-1479.
16
17.Morris GM, Doodsell DS, Holliday RS, Huey R, Hart WE, Belew RK, et al. Automated docking using a Lamarckian genetic algorithm and an empirical binding free energy function. J Comput Chem 1998; 19:1639-1662.
17
18.Hosseinzadeh H, Ramezani M, Salmani G. Antinociceptive, anti-inflammatory and acute toxicity effects of Zataria multiflora Boiss extracts in mice and rats. J Ethnopharmacol 2000; 73:379-385.
18
19.Rowlinson SW, Kiefer JR, Prusakiewicz JJ, Pawlitz JL, Kozak KR, Kalgutkar AS, et al. A novel mechanism of cyclooxygenase-2 inhibition involving interactions with Ser-530 and Tyr-385. J Biol Chem 2003; 278:45763-45769.
19
20.Wallace AC, Laskowski RA, Thornton JM. LIGPLOT: a program to generate schematic diagrams of protein- ligand interactions. Protein Eng 1995; 8:127-134.
20
ORIGINAL_ARTICLE
Amlodipine Ameliorates Up-Regulation of ET-1 in Left Ventricle of Hypercholesterolemia Rabbits
Objective(s)
In addition to antihypertensive effects, amlodipine may exhibit cardiovascular protective effects in heart tissue. The aim of this study was to evaluate the effects of amlodipine and/or high cholesterol diet on blood, heart tissue concentration and mRNA expression of endothelin-1 (ET-1) in male New Zealand white rabbits.
Materials and Methods
A total of 40 male New Zealand rabbits were divided into four groups: the normal control group, normal group receiving amlodipine, high-cholesterol diet group and high-cholesterol diet with amlodipine group. After 8 weeks, all the animals anesthetized and blood or tissues samples were collected.
Results
After 8 weeks of a high cholesterol diet, the group with such a diet had a significantly higher ratio of left ventricle (LV) weight to body weight than the control group (P= 0.0001). After treatment with amlodipine for 8 weeks, ET-1 level was reduced considerably in comparison with the control (P= 0.01) and high- cholesterol diet groupes (P= 0.01). Amlodipine consumption caused significant reduction (P= 0.01) in the level of ET-1 in heart tissues of high-cholesterol diet group but it had no remarkable effect on the reduction of heart tissue ET-1 in amlodipine group compared with the control group.
Conclusion
The present study demonstrates that ventricular prepro-ET-1 mRNA quantitatively increases in the high- cholesterol diet rabbits which results in development of ventricular hypertrophy. It seems that the treatment with amlodipine retards the progression of LV hypertrophy through attenuation of ET-1 levels independent of lipid changes.
https://ijbms.mums.ac.ir/article_5122_3147dcb9e4b91d7e840f43dd6bb9db80.pdf
2010-10-01
232
238
10.22038/ijbms.2010.5122
Amlodipine
Endothelin-1
Hyperlipidemias
Hypertrophy
Rabbits
Iraj
Salehi
irsalehi@yahoo.com
1
Department of Physiology, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
AUTHOR
Safar
Farajnia
farajnias@tbzmed.ac.ir
2
Biotechnology Research Center & Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Mustafa
Mohammadi
m.mohammadin@yahoo.com
3
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Masoud
Sabouri Ghannad
sabouri@umsha.ac
4
Department of Microbiology, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
LEAD_AUTHOR
1.James PT, Rigby N, Leach R. International obesity task Force. The obesity epidemic, metabolic syndrome and future prevention strategies. Eur J Cardiovasc Prev Rehabil 2004; 11:3-8.
1
2.Alpert MA. Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome. Am J Med Sci 2001; 321:225-236.
2
3.Hubert HB, Feinleib M, McNamara PM, Casteelii WP. Obesity as an independent risk factor for cardiovascular disease: a 26-year follow-up of participants in the Framingham Heart Study. Circulation 1983; 67:9 68-77.
3
4.Kenchaiah S, Evans JC, Levy D, Wilson PW, Benjamin EJ, Larson MG, et al. Obesity and the risk of heart failure. N Engl J Med 2002; 347:305-313.
4
5.Sadoshima J, Izumo S. The cellular andmolecular response of cardiac myocytes to mechanical stress. Annu Rev Physiol 1997; 59:551-571.
5
6.Castelli WP, Anderson K. A population at risk: prevalence of high cholesterol levels in hypertensive patients of the Framingham Study. Am J Med 1986; 23-32.
6
7.Bohn F, Johansson B, Hedin U, Alving K, Pernow J. Enhanced vasoconstrictor effect of big endothelin-1 patients with athrosclerosis : relation to conversion to endothelin - 1 .Atherosclerosis 2002; 160:215-222.
7
8.Lerman A, Webster MW, Chesebro JH, Edwards WD, Wei CM, Fuster V, et al. Circulating and tissue endothelin immnoreactivity in hypercholesterolemic pigs. Circulation 1993; 88:2923-2928.
8
9.Haak T, Marz W, Jungmann E, Hausser S, Siekmeier R, Gross W, et al. Elevated endothelin levels in patients with hyperlipidemia. Clin Investig 1994; 72:580-584.
9
10.Yue TL, Gu JL, Wang C, Reith AD, Lee JC, Mirabile RC, et al. Extracellular signal-regulated kinase plays an essential role in hypertrophic agonists, endothelin-1 and phenylephrine-induced cardiomyocyte hypertrophy. J Biol Chem 2000; 275:37895-378901.
10
11.Davenport AP,Maguire JJ. Of mice and men: advances in endothelin research and first antagonist gains FDA approval. Trends Pharmacol Sci 2002; 23:155-157.
11
12.Waters D, Lesperance J, Francetich M, Causey D, Theroux P, Chiang YK, et al. A controlled clinical trial to assess the effect of a calcium channel blocker on the progression of coronary atherosclerosis. Circulation 1990; 82:1940-1953.
12
13.Pitt B, Byington RP, Furberg CD, Hunninghake DB, Mancini GB, Miller ME, et al. Effect of amlodipine on the progression of atherosclerosis and the occurrence of clinical events. PREVENT Investigators. Circulation 2000; 102:1503-1510.
13
14.Jukema JW, Zwinderman AH, van Boven AJ, Reiber JH, Van der Laarse A, Lie KI, et al. Evidence for a synergistic effect of calcium channel blockers with lipid-lowering therapy in retarding progression of coronary atherosclerosis in symptomatic patients with normal to moderately raised cholesterol levels. The REGRESS Study Group. Arterioscler Thromb Vasc Biol 1996; 16:425-430.
14
15.Catapano AL. Calcium antagonists and atherosclerosis. Experimental evidence. Eur Heart J 1997; 18:A80-86.
15
16.Bellosta S, Bernini F. Lipophilic Calcium Antagonists in Antiatherosclerotic Therapy. Current Atherosclerosis Reports 2000; 2:76-81.
16
17.Mitani H, Takimoto M, Bandoh T, Kimura M. Increases of vascular endothelin-converting enzyme activity and endothelin-1 level on atherosclerotic lesions in hyperlipidemic rabbits. Eur J Pharmacol 2000; 387:313-319.
17
18.Sugden PH. Signaling pathways activated by vasoactive peptides in the cardiac myocyte and their role in myocardial pathologies. J Card Fail 2002; S359-369.
18
19.Ito H, Hirata Y, Adachi S, Tanaka M, Tsujino M, Koike A, et al.Endothelin-1 is an autocrine/paracrine factor in the mechanism of angiotensin II-induced hypertrophy in cultured rat cardiomyocytes. J Clin Invest 1993; 92:398-403.
19
20.Ishiye M, Umemura K, Uematsu T, Nakashima M. Angiotensin AT1 receptor-mediated attenuation of cardiac hypertrophy due to volume overload: involvement of endothelin. Eur J Pharmacol 1995; 280:11-7.
20
21.Warnholtz A, Nickenig G, Schulz E, Macharzina R, Brasen JH, Skatchkov M, et al. Increased NADH-oxidase- mediated superoxide production in the early stages of atherosclerosis: evidence for involvement of the renin- angiotensin system. Circulation 1999; 99:2027-2033.
21
22.Hu CT, Chang HR, Hsu YH, Liu CJ, Chen HI. Ventricular hypertrophy and arterial hemodynamics following deprivation of nitric oxide in rats. Life Sci 2005; 78:164-173.
22
23.Castro GJ, Bhatnagar A. Effect of extracellular ions and modulators of calcium transport on survival of tert- butyl hydroperoxide exposed cardiac myocytes. Cardiovasc Res 1993; 27:1873-1881.
23
24.Takemoto M, Node K, Nakagami H, Liao Y, Grimm M, Takemoto Y, et al. Statins as antioxidant therapy for preventing cardiac myocyte hypertrophy. J Clin Invest 2001; 108:1429-1437.
24
25.Lee TM, Chou TF, Tsai CH. Association of pravastatin and left ventricular mass in hypercholesterolemic patients: role of 8-iso-prostaglandin f2alpha formation. J Cardiovasc Pharmacol 2002; 40:868-874.
25
ORIGINAL_ARTICLE
Effects of Epigallocatechin Gallate on Tissue Lipid Peroxide Levels in Traumatized Spinal Cord of Rat
Objective(s)
Recent studies revealed the neuroprotective effects of epigallocatechin gallate (EGCG) on a variety of neural injury .The purpose of this study was to determine the effects of EGCG on the tissue lipid peroxidation after spinal cord injury (SCI).
Materials and Methods
Rats were randomly divided into four groups of 7 rats each as follows: sham-operated group, trauma group, and EGCG-treatment groups (50 mg/kg, i.p., immediately and 1 hr after SCI). The rats were euthanized 24 hr after injury and then, spinal cord samples were taken for determination of malodialdehyde levels, as an indicator of lipid peroxidation.
Results
The results showed that MDA levels were significantly decreased in EGCG-treatment groups.
Conclusion
On the basis of these findings, we propose that EGCG may be effective in protection of spinal cord tissue from injury.
https://ijbms.mums.ac.ir/article_5123_ef6c770a74fd60c4905f6b1dfc8692a4.pdf
2010-10-01
239
242
10.22038/ijbms.2010.5123
Antioxidants
Epigallocatechin gallate
Lipid Peroxides
Spinal cord injuries
Ali Reza
Khalatbary
khalat90@yahoo.com
1
Razi Herbal Medicine Research Center, Lorestan University of Medical Sciences, Khoramabad, Iran
LEAD_AUTHOR
Hasan
Ahmadvand
hassan-a46@yahoo.com
2
Department of Biochemistry, Lorestan University of Medical Sciences, Khoramabad, Iran
AUTHOR
1.Amar AP, Levy ML. Pathogenesis and pharmacological strategies for mitigating secondary damage in acute spinal cord injury. Neurosurgery 1999; 44:1027-1039.
1
2.Hall ED. The role of oxygen radicals in traumatic injury: clinical implications. J Emerg Med 1993; 11:31-36.
2
3.Popovich PG, Wei P, Stokes BT. Cellular inflammatory response after spinal cord injury in Sprague-Dawley and Lewis rats. J Comp Neurol 1997; 377:443-64.
3
4.Popovich PG, Stokes BT, Whitacre CC. Concept of autoimmunity following spinal cord injury: possible roles for T lymphocytes in the traumatized central nervous system. J Neurosci Res 1996 ; 45:349-63.
4
5.Mautes AE, Weinzierl MR, Donovan F, Noble LJ. Vascular events after spinal cord injury: contribution to secondary pathogenesis. Phys Ther 2000; 80:678-687.
5
6.Sutherland BA, Rahman RM, Appleton I. Mechanisms of action of green tea catechins, with a focus on ischemia-induced neurodegeneration. J Nutr Biochem 2006; 17:291-306.
6
7.Kimura M, Umegaki K, Kasuya Y, Sugisawa A, Higuchi M. The relation between single/double or repeated tea catechin ingestions and plasma antioxidant activity in humans. Eur J Clin Nutr 2002; 56:1186-1193.
7
8.Choi YB, Kim YI, Lee KS, Kim BS, Kim DJ. Protective effect of epigallocatechin gallate on brain damage after transient middle cerebral artery occlusion in rats. Brain Res 2004; 1019:47-54.
8
9.Wei H, Wu YC, Wen CY, Shieh HY. Green tea polyphenol (-)-epigallocatechin gallate attenuates the neuronal NADPH-d/nNOS expression in the nodose ganglion of acute hypoxic rats. Brain Res 2004; 999:73-80.
9
10.Lin AM, Chyi BY, Wu LY, Hwang LS, Ho LT. The antioxidative property of green tea against iron-induced oxidative stress in rat brain. Chin J Physiol 1998; 41:189-194.
10
11.He M, Zhao L, Wet MJ, Yao WF, Zhao HS, Chen FJ. Neuroprotective effects of (-)-Epigallocatechin-3-gallate on aging mice induced by D- galactose. Biol Pharm Bull 2009; 32:55-60.
11
12.Paterniti I, Genovese T, Crisafulli C, Mazzon E, Dipaola R, Galuppo M, et al. Treatment with green tea extract attenuates secondary inflammatory response in an experimental model of spinal cord trauma. Naunyn Schmiedebergs Arch Pharmacol 2009; 380:179-192.
12
13.Mihara S, Uchiyama M. Determination of malonaldehyde precursor in tissues by thiobarbituric acid test. Anal Biochem 1978; 86:271-278.
13
14.Liu XZ, Xu XM, Hu R, Du C, Zhang SX, Mcdonald JW, et al. Neuronal and glial apoptosis after traumatic spinal cord injury. J Neurosci 1997; 17:5395-406.
14
15.Kwon BK, Tetzlaff W, Grauer JN, Beiner J, Vaccaro AR. Pathophysiology and pharmacologic treatment of acute spinal cord injury. Spine J 2004; 4:451-464.
15