Résumé
<p><b>OBJECTIVE</b>To investigate the expression and pathobiological implications of angiotensin II type 1 receptor (AT1R) in development of myocardial fibrosis of rats.</p><p><b>METHODS</b>Rat myocardial necrosis model was established using isoproterenol injection (15 mg/kg). Rat serum aspartate transaminase (AST), lactate dehydrogenase (LDH), creatine kinase (CK) and creatine kinase isoenzymes (CK-MB) were detected by MD-100 automatic biochemical analyzer. Masson staining was used to evaluate the morphological changes. The expression of AT1R protein was determined by immunohistochemistry and its mRNA expression was analyzed by RT-PCR. The expression of collage type I and III was determined by immunohistochemistry.</p><p><b>RESULTS</b>Serum LDH, CK and CK-MB reached their peaks at 4 h (chi2 = 16.90, P < 0.05), and AST achieved its peak in 6 h (chi2 = 16.90, P < 0.05). AT1R mRNA expression was increased 2 - 12 h after isoproterenol injection, but no statistical significance (P > 0.05) was observed comparing with the control. However, a significant AT1R mRNA increase was present at 24 h and decreased gradually after 48 h, and back to the control level after 3 weeks. Protein expression of AT1R increased proportionally with the severity of the fibrosis.</p><p><b>CONCLUSIONS</b>AT1R mRNA and protein expressions increase significantly during myocardial ischemia, and is closely correlated with the fibrosis. These findings indicate that AT1R may play an important role in the pathogenesis of myocardial fibrosis.</p>
Sujets)
Animaux , Mâle , Rats , Aspartate aminotransferases , Génétique , Cardiomyopathies , Métabolisme , Différenciation cellulaire , Physiologie , Creatine kinase , Génétique , Fibrose , Métabolisme , Immunohistochimie , Isoprénaline , L-Lactate dehydrogenase , Génétique , Métabolisme , Infarctus du myocarde , Anatomopathologie , Ischémie myocardique , Anatomopathologie , Myocarde , Métabolisme , ARN messager , Métabolisme , Rat Wistar , Récepteur de type 1 à l'angiotensine-II , Génétique , Métabolisme , RT-PCRRésumé
<p><b>OBJECTIVE</b>To investigate the ameliorative effect of ginseng glycopeptide on cross-linking of rat tail tendon collagen.</p><p><b>METHOD</b>ELISA was used to determine the inhibitory effect of ginseng glycopeptide on cross-linking of rat tail tendon collagen in vitro. After ginseng glycopeptide was intraperitoneally administrated to streptozotocin-induced diabetic rats for 12 weeks, the acid solubility, limited pepsin degradation properties and solubility in SDS-2-mercaptoethanol of the rat tail tendon collagen were determined, and the effect of ginseng glycopeptide on the tail tendon collagen cross-linking was evaluated.</p><p><b>RESULT</b>Ginseng glycopeptide inhibited significantly the cross-linking of rat tail tendon collagen in vitro. The solubility of the tail tendon collagen (in acid, pepsin and SDS-2-mercaptoethanol) was markedly decreased in diabetic rats and ginseng glycopeptide-treated diabetic rats had significantly an increase in the collagen solubility in the above-mentioned solutions, suggesting that ginseng glycopeptide decreased severity of the collagen cross-linking.</p><p><b>CONCLUSION</b>Ginsengglycopeptide exhibits an significantly ameliorative effect on cross-linking of rat tail tendon collagen.</p>