作者: Juan Zhang , Xiao-Xing Li , Hong-Jun Bian , Xiao-Bo Liu , Xiao-Ping Ji
DOI: 10.1016/J.CCA.2008.11.016
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摘要: Abstract Background Recent studies have demonstrated that Rho-kinase has been proposed to play an important role in the pathogenesis of heart ischemia/reperfusion (I/R) injury. However, mechanism mediated cardiomyocyte apoptosis I/R is still not thoroughly understood. Method Studies were performed with female Wistar rats. Results Ischemia followed by reperfusion caused a significant increase Rho-kinase, c-Jun NH2-terminal kinase (JNK) and apoptosis-inducing factor (AIF) activity. Administration fasudil, inhibitor decreased myocardial infarction size from 59.89 ± 3.83% 38.62 ± 2.66% ( P Conclusion The inhibition reduced cell vivo via suppression JNK-mediated AIF translocation.