Role of Rho-kinase in remote ischemicpostconditioning against myocardial ischemia/reperfusion injury
10.3969/j.issn.1001-1978.2017.10.012
- VernacularTitle:Rho激酶在远距缺血后处理抗心肌缺血/再灌注损伤中的作用
- Author:
Feng MIN
;
Xianjie JIA
;
Hongjie SHI
;
Jing HU
;
Zhiyuan HU
;
Qin GAO
;
Ying YU
- Keywords:
Rho-kinase;
remote ischemic postconditioning;
ischemia/reperfusion;
cardioprotection;
fasudil;
lysophosphatidic acid
- From:
Chinese Pharmacological Bulletin
2017;33(10):1387-1392
- CountryChina
- Language:Chinese
-
Abstract:
Aim To explore the role of Rho-kinase in remote ischemic postcondi-tioning and its possible mechanism.Methods Thirty male Sprague-Dawley rats were divided into five groups(n=6): sham group(Sham), ischemia/reperfusion group(I/R), remote ischemic postconditioning group(RIPostC), I/R with Rho-kinase inhibitor fasudil group(I/R+Fas) and RIPostC with Rho-kinase activator lysophosphatidic acid group(RIPostC+LPA).Throughout the whole process of experiment, mean arterial pressure(MAP), heart rate(HR) and Ⅱ lead electrocardiogram were continuously monitored.At the end of the reperfusion, plasma creatine kinase(CK) and lactate dehydrogenase(LDH) were measured.Myocardial histopathologic changes were observed by hematoxylin and eosin(HE) staining.Infarct size was measured using 2,3,5-triphenyltetrazolium chloride(TTC) staining.The expressions of phospho-myosin light chain(p-MLC) were detected with Western blot analysis.Results Compared with Sham group, the MAP and HR of other groups decreased, while the amplitude of ST segment increased.Compared with I/R group, MAP and HR increased, the amplitude of ST segment decreased, plasma CK and LDH activity decreased, myocardial pathological morphology and infarct size were improved significantly, infiltration of inflammatory cells was reduced, and the expression of p-MLC decreased in RIPostC and I/R+Fas group.Compared with RIPostC group, RIPostC+LPA group attenuated the effects of RIPostC, and the recovery of the above indicators were inhibited.Conclusion Rho-kinase signaling pathway might mediate remote ischemia postconditioning against myocardial ischemia/reperfusion injury.
