The effect of protease-activated receptor2 on rat apoptotic cardiomyocytes underwent ischemia reperfusion injury
Tong, X.-H.; Ding, J.-W.; Yang, J.; Liu, C.-Q.; Zhang, Y.; Li, S.; Li, W.-H.; Li, L.
Zhonghua Xin Xue Guan Bing Za Zhi 37(9): 832-836
2009
ISSN/ISBN: 0253-3758 PMID: 20128384 Document Number: 629420
To investigate the effect of protease-activated receptor 2 (PAR-2) on rat apoptotic cardiomyocytes underwent ischemia reperfusion (I/R) injury. Healthy male Sprague-Dawley rats were randomly divided into five groups (n = 8 each): sham-operation group, I/R (ligating the left coronary artery for 30 minutes and followed by 120 minutes reperfusion) group and three SLIGRL-NH2 groups treated with intravenous PAR-2 agonist SLIGRL-NH2 at different doses (0.5, 1, 3 mg/kg) 5 minutes before reperfusion. Apoptic cardiomyocytes was detected by TUNEL staining and by DNA ladder on agarose gel electrophoresis. Bax and Bcl-2 expression in myocardium was analyzed by immunohistochemical technique. The mRNA expression of PAR-2 was determined by Real-time quantitative polymerase chain reaction (RT-PCR). (1) The apoptosis index and the expression of Bcl-2 and Bax were significantly increased in IR group and SLIGRL-NH2 groups than those in sham group (P < 0.05-0.01). (2) Compared with I/R group, the apoptosis index and the expression of Bax were significantly reduced while the expression of Bcl-2 and PAR-2 mRNA were significantly upregulated by SLIGRL-NH2 in a dose-dependent manner. (3) DNA Agarose gel electrophoresis demonstrated that DNA ladder existed in I/R and 0.5 mg/kg SLIGRL-NH2 group, but not in 1, 3 mg/kg SLIGRL-NH2 groups. PAR-2 agonist SLIGRL-NH2 could reduce myocardial apoptosis by upregulating the Bcl-2 and PAR-2 mRNA level and downregulating Bax expression in a dose-dependent manner in this rat I/R model.