Paper Information

Title: 

THE ROLE OF ANGIOTENSIN TYPE 2 (AT2) RECEPTOR IN BLEOMYCIN-INDUCED PULMONARY FIBROSIS IN MICE

Type: POSTER
Author(s): SAFAEIAN L.*,JAFARIAN DEHKORDI A.,MIRMOHAMMAD SADEGHI H.,AFSHAR MOGHADAM N.,ALAVI S.A.
 
 *DEPT. OF PHARMACOLOGY AND TOXICOLOGY, ISFAHAN UNIVERSITY OF MEDICAL SCIENCES
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2007Volume 18
 
 
Abstract: 

Introduction: Angiotensin plays an important role in the pathogenesis of pulmonary fibrosis. In spite of antifibrotic effects of AT2 receptor in cardiac and renal fibrosis, its role in pulmonary fibrosis is not fully understood. Therefore, we sought to determine the role of this receptor in pulmonary fibrosis using bleomycin-induced lung fibrosis in mice.
Methods: For establishing the animal model of pulmonary fibrosis, bleomycin (0.075 U) was administrated by surgical intratracheal instillation under anesthesia with ketamine (75mg/kg) in NMRI mice. AT2 receptor agonist [CGP42112A (0.25, 0.5, 1 and 2 mg/kg)] and antagonist [PD123319 (0.5, 1, 2 and 3mg/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) and histological examination (by Masson's trichrome staining).
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 from 182.4+15
μg/lung to 143.8+10.2 μg/lung. PD123319 failed to reduce the pulmonary fibrotic changes induced by bleomycin.
Conclusion: AT2 receptors could ameliorate the pulmonary fibrosis by reduction of collagen deposition and may be useful in the treatment of pulmonary fibrosis.

 
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