标题：Rho-kinase signaling pathway promotes the expression of PARP to accelerate cardiomyocyte apoptosis in ischemia/reperfusion
作者：Bian, Hongjun; Zhou, Yi; Yu, Bin; Shang, Deya; Liu, Fuli; Li, Bin; Qi, Jianni
作者机构：[Bian, Hongjun; Zhou, Yi; Yu, Bin; Shang, Deya; Liu, Fuli] Shandong Univ, Shandong Prov Hosp, Dept Emergency, Jinan 250021, Shandong, Peoples R China. 更多
通讯作者地址：[Qi, JN]Shandong Univ, Shandong Prov Hosp, Cent Lab, 324 Jingwu Rd, Jinan 250021, Shandong, Peoples R China.
来源：MOLECULAR MEDICINE REPORTS
关键词：ROCK; PARP; ERK; ischemia/reperfusion
摘要：It has been previously reported that Rho-kinase (ROCK) and poly ADP-ribose polymerase (PARP) serve critical roles in myocardial ischemia/reperfusion (I/R) injury. Studies have additionally demonstrated that the activation of ROCK and the expression of PARP are increased in I/R. However, the effect and mechanism of the two proteins remains to be fully elucidated in I/R. In addition, whether they can be influenced by each other is unclear. In the present study, it was demonstrated that ischemia followed by reperfusion resulted in a significant increase in ROCK and PARP. In addition, Y-27632 (ROCK inhibitor) and 3-aminobenzamide (3-AB; PARP inhibitor) pretreatment rescued myocardial infarction size and cardiomyocyte apoptosis. The inhibitory role of Y-27632 was observed to be superior to that of the 3-AB group. In addition, Y-27632 and 3-AB diminished extracellular signal-related kinase (ERK) phosphorylation and the production of tumor necrosis factor a and interleukin 6. Overall, the results of the present study suggested that the inhibition of ROCK leads to reduced myocardial infarction size and cardiomyocyte apoptosis via the PARP/ERK signaling pathway.