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" The role of angiotensin type 2 receptor( AT2) in bleomycin-induced apoptosis, bcl-2 and bax genes expression and pulmonary fibrosis in mice "
/صفائیان نائینی، لیلا
; Abbas Jafarian Dehkordi, Mohammad Rabbani, Hamid Mir Mohammad Sadeghi
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Isfahan University of Medical Sciences
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| Document Type
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Latin Dissertation
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English
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| Record Number
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102650
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| Doc. No
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T10665
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| Call number
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QU,68,S128r,2007
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| Main Entry
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Safaeian Naeini, Leila
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| Title & Author
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The role of angiotensin type 2 receptor( AT2) in bleomycin-induced apoptosis, bcl-2 and bax genes expression and pulmonary fibrosis in mice/صفائیان نائینی، لیلا
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| College
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Schools, Phamacy
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| Date
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, 2007
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| Degree
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Pharmacology, Ph.D
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| Page No
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XIII, 142 p.:ill( som col ), diag
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This Thesis is also a research Project with project ID 83296
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Orginal Works
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| Abstract
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Introduction: Angiotensin plays an important role in the pathogenesis of pulmonary fibrosis and apoptosis. In spite of antifibrotic effects of AT2 receptor in cardiac and renal fibrosis, its role in pulmonary fibrosis has not been fully understood. Therefore, we sought to determine the role of this receptor in pulmonary fibrosis and apoptosis using bleomycin-induced lung fibrosis in mice. Methods: Bleomycin (0.075 U) was administrated by surgical i.t. instillation in NMRI mice. AT2 receptor agonist [CGP42112A (0.25, 0.5, 1 and 2 mg/kg)] and antagonist [PD123319 (0.5, 1, 2 and 3 mg/kg)] were instilled by pharyngeal aspiration technique, two days before the bleomycin instillation and continued three times weekly for 2 weeks. Control mice were instilled with the same volume of saline. After 2 weeks, lungs were analyzed for collagen content (by spectrophotometric assay of hydroxyproline), histological examination, detection and quantitation of apoptosis (by TUNEL assay) and apoptosis regulatory markers including bcl-2 and bax (by biotin-streptavidin immunohistochemistry method). Results: CGP42112A attenuated the histologic changes and significantly (p < 0.05)) reduced the increase in total lung collagen induced by bleomycin at dose of 1 mg/kg to 143.8 + 10.2 [Leung, but did not significantly reduced lung epithelial apoptosis. PD123319 failed to reduce the fibrotic changes. Both agonist and antagonist reduced the bax/bc1-2 expression ratio in the alveolar epithelial cells and myofibroblasts, and enhanced it in polymorphonuclears. Conclusion: AT2 receptors could ameliorate the pulmonary fibrosis by reduction of collagen deposition and decreasing the susceptibility of alveolar epithelial cells to apoptosis, and may be useful in the treatment of pulmonary fibrosis..
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| Descriptor
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1. Receptors, Angiotensin.- Descriptors: Pulmonary Fibrosis
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Angiotensins
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Bleomycin
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Aspiration
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Receptor Angiotensin Type 2
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Jafarian Dehkordi, Abbas, Supervisor
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Rabbani, Mohammad, Supervisor
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Mir Mohammad Sadeghi, Hamid, Supervisor
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| Translated Title Supplied by Cataloguer
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بررسی نقش رسپتور AT2 آنژیوتانسین در آپوپتوز، بیان ژن های bcl-2 و bax و فیبروز ریوی ناشی از بلئومایسین در موش
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