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:Qi, JN
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
出版年:2017
卷:16
期:2
页码:2002-2008
DOI:10.3892/mmr.2017.6826
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.
收录类别:SCOPUS;SCIE
WOS核心被引频次:1
Scopus被引频次:1
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-85022331684&doi=10.3892%2fmmr.2017.6826&partnerID=40&md5=7b7944e0b49a744acd8681d18ce93079
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