Han Yongli, Chen Song, Wang Hua, Peng Xing-Ming
College of Acupuncture and Orthopedics, Hubei University of Traditional Chinese Medicine, Wuhan, Hubei 430061, China.
Hubei Collaborative Innovation Center for Acupuncture Treatment, Wuhan, Hubei 430061, China.
Evid Based Complement Alternat Med. 2021 Mar 8;2021:8827891. doi: 10.1155/2021/8827891. eCollection 2021.
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.
电针预处理对心肌缺血/再灌注(I/R)损伤具有有益作用。然而,电针作用的分子机制尚未完全明确。本研究旨在探讨电针预处理对大鼠心肌缺血再灌注损伤(MIRI)的保护作用及其凋亡相关机制。对大鼠进行体内心肌缺血再灌注、电针预处理或静脉注射拮抗剂。检测心功能、梗死面积和心肌细胞凋亡情况。同时,还检测了MKK3、MKK6、p38MAPK、Bax、Bcl-2和Caspase-3的表达。我们发现电针预处理显著减小了梗死面积,减少了心肌细胞凋亡,并增强了心功能。电针预处理降低了Bax、Caspase-3、MKK3、MKK6、p38MAPK、Bax和Caspase-3的表达。总之,电针预处理通过RhoA/p38MAPK途径下调MKK3、MKK6和p38MAPK的表达。电针预处理通过下调MKK3、MKK6和p38MAPK的表达保护MIRI大鼠免于凋亡,从而减少Bax、Caspase-3的表达并上调Bcl-2的表达,其机制与miR-133a-5p介导的RhoA/p38MAPK途径密切相关。