诱导型一氧化氮合成酶参与大鼠心脏缺血后处理延迟相的保护作用

doi:10.6040/j.issn.1671-7554.0.2015.829

摘要/Abstract

摘要： 目的探讨心肌缺血后处理的延迟相保护作用,以及诱导型一氧化氮合成酶(iNOS)在延迟相保护作用中的意义。方法 160只大鼠随机分为5组:缺血再灌注组(I/R组)、缺血后处理组(IPO组)、缺血后处理+1400W(iNOS阻断剂)组(IPO+1400W组)、缺血再灌注+1400W组(I/R+1400W组)和假手术组,每组32只,分别接受3、24、48、72 h再灌注(每时间点8只)。测定各组心肌梗死面积与肌酸激酶(CK)活性,检测磷酸化内皮型一氧化氮合酶(p-eNOS)与iNOS的表达。结果再灌注3 h,IPO组与I/R组相比,左室梗死面积明显减少［(18.0±2.3)% vs(30.7±3.1)%, P<0.05］;再灌注72 h,IPO组与I/R组相比梗死面积差异有统计学意义［(25.7±1.1)% vs(34.9±0.8)%, P<0.05］;各组CK活性的差异与梗死面积的差异一致。再灌注3、24 h,IPO组与I/R组相比,p-eNOS表达增多;再灌注48、72 h,IPO组iNOS表达增多。结论缺血后处理具有延迟相心肌保护作用,iNOS在后处理延迟相心肌保护中必不可少。

关键词: 缺血再灌注损伤, 诱导型一氧化氮合成酶, 延迟相心肌保护, 缺血后处理, 内皮型一氧化氮合成酶

Abstract: Objective To investigate the delayed cardioprotective effects of ischemic preconditioning(IPO)and the role of inducible nitric oxide synthase(iNOS)in the late phase of IPO. Methods A total of 160 rats were randomized into 5 groups: I/R group, IPO group, IPO+1400W(iNOS inhibitor)group, I/R+1400W group and sham-operated(sham)group. Animals in each group received 3, 24, 48 or 72 h of reperfusion after ischemia(n=8 per each time point). Cardio-infarct size and creatine kinase(CK)activity were measured respectively. Western blotting was used to assess the expressions of phosphorylated endothelial nitric oxide synthase(p-eNOS)and iNOS in the heart. Results At reperfusion 3 h, in the IPO group, the infarct size of left ventricle(LV)decreased significantly compared with I/R group［(18.0±2.3)% vs(30.7±3.1)%, P<0.05). At reperfusion 72 h, the difference between IPO group and I/R group in infarct size was obvious［(25.7±1.1)% vs(34.9±0.8)%, P<0.05］. Difference in the CK activity was positively correlated with the difference in infarct size in all groups. IPO increased p-eNOS levels at R 3 h and R 24 h 山东大学学报 (医学版)54卷2期 -李欣,等.诱导型一氧化氮合成酶参与大鼠心脏缺血后处理延迟相的保护作用 \=-and iNOS levels at R 48 h and R 72 h. Conclusion IPO has delayed cardioprotective effects on myocardial infarction, and iNOS plays a critical role in the delayed effects against heart injury.

Key words: Ischemic postconditioning, Ischemia-reperfusion injury, Endothelial nitric oxide synthase, Inducible nitric oxide synthase, Delayed cardioprotective effect

中图分类号:

R654

李欣,王公明,王红,王岩,张立功,张乐,刘蓓,张孟元. 诱导型一氧化氮合成酶参与大鼠心脏缺血后处理延迟相的保护作用[J]. 山东大学学报（医学版）, 2016, 54(2): 16-20.

LI Xin, WANG Gongming, WANG Hong, WANG Yan, ZHANG Ligong, ZHANG Le, LIU Bei, ZHANG Mengyuan. Inducible nitric oxide synthase contributes to the delayed cardioprotection of ischemic postconditioning in rats[J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2016, 54(2): 16-20.

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