蛋白酶激活受体-2对缺血再灌注大鼠心肌细胞凋亡的影响 |
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引用本文: | 童晓红,丁家望,杨俊,刘朝奇,张艳,李松,李稳慧,李莉.蛋白酶激活受体-2对缺血再灌注大鼠心肌细胞凋亡的影响[J].中华心血管病杂志,2009,37(6):832-836. |
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作者姓名: | 童晓红 丁家望 杨俊 刘朝奇 张艳 李松 李稳慧 李莉 |
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作者单位: | 三峡大学第一临床医学院宜昌市中心人民医院心内科,443003;三峡大学分子生物所; |
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摘 要: | Objective To investigate the effect of protease-activated receptor2 (PAR-2) on rat apoptotic cardiomyocytes underwent iachemia reperfusion (I/R) injury. Methods 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). Results (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 upregnlated 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. Conclusions PAR-2 agonist SLIGRL-NH2 could reduce myocardial apoptosis by upregulating the Bcl-2 and PAR-2 mRNA level and downregnlating Bax expression in a dose-dependent manner in this rat I/R model.
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关 键 词: | 心肌再灌注损伤 受体 细胞凋亡 |
The effect of protense-activated receptor2 on rat apoptotic cardiomyocytes underwent ischemia reperfnsion injury |
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Abstract: | |
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Keywords: | PAR-2Myocardial reperfusion injuryReceptorPAR-2Apoptosis |
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