Electroacupuncture Pretreatment Regulates Apoptosis of Myocardial Ischemia-Reperfusion Injury in Rats Through RhoA/p38MAPK Pathway Mediated by miR-133a-5p

被引:13
作者
Han, Yongli [1 ]
Chen, Song [2 ,3 ]
Wang, Hua [1 ]
Peng, Xing-ming [4 ]
机构
[1] Hubei Univ Tradit Chinese Med, Coll Acupuncture & Orthoped, Wuhan 430061, Hubei, Peoples R China
[2] Hubei Collaborat Innovat Ctr Acupuncture Treatmen, Wuhan 430061, Hubei, Peoples R China
[3] Second Peoples Hosp Jingzhou, Jingzhou 434099, Hubei, Peoples R China
[4] Hubei Univ Tradit Chinese Med, Huangjiahu Hosp, Inst Internal Med, Wuhan 430065, Hubei, Peoples R China
关键词
ENDOTHELIAL-CELL MIGRATION; INFARCTION; EXPRESSION; DELIVERY; RHOA;
D O I
10.1155/2021/8827891
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
The electroacupuncture (EA) pretreatment possesses a beneficial effect on myocardial ischemia/reperfusion (I/R) injury. However, the molecular mechanism of the EA effect is not fully understood. The study aimed to explore the protective effect of EA pretreatment on myocardial ischemia-reperfusion injury (MIRI) and apoptosis-related mechanisms in rats. Rats underwent in vivo myocardial ischemia-reperfusion, EA pretreatment, or intravenous injection of antagomirs. Cardiac function, infarct area, and myocardial cell apoptosis were measured. Meanwhile, the expressions of MKK3, MKK6, p38MAPK, Bax, Bcl-2, and Caspase-3 were also detected. We found that EA pretreatment significantly reduced infarct area and myocarpal cell apoptosis and enhanced cardiac function. EA pretreatment decreased the expression of Bax, Caspase-3, MKK3, MKK6, p38MAPK, Bax, and Caspase-3. In conclusion, The EA pretreatment down regulated the expression of MKK3, MKK6, and p38MAPK through the RhoA/p38MAPK pathway. EA pretreatment protect MIRI rats from apoptosis by down regulating the expression of MKK3, MKK6, and p38MAPK, thereby reducing the expression of Bax, Caspase-3 and up regulating the expression of Bcl-2, which mechanism is closely related to the RhoA/p38MAPK pathway mediated by miR-133a-5p.
引用
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页数:13
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