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

Yongli Han; Song Chen; Hua Wang; Xing-Ming Peng

doi:10.1155/2021/8827891

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

Evid Based Complement Alternat Med. 2021 Mar 8:2021:8827891. doi: 10.1155/2021/8827891. eCollection 2021.

Authors

Yongli Han^#¹, Song Chen^#^{2

3}, Hua Wang¹, Xing-Ming Peng⁴

Affiliations

¹ College of Acupuncture and Orthopedics, Hubei University of Traditional Chinese Medicine, Wuhan, Hubei 430061, China.
² Hubei Collaborative Innovation Center for Acupuncture Treatment, Wuhan, Hubei 430061, China.
³ Second People's Hospital of Jingzhou, Jingzhou, Hubei 434099, China.
⁴ Institute of Internal Medicine, Huangjiahu Hospital of Hubei University of Traditional Chinese Medicine, Wuhan, Hubei 430065, China.

^# Contributed equally.

Abstract

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.