Cardioprotective Effect of Electroacupuncture Pretreatment on Myocardial Ischemia/Reperfusion Injury via Antiapoptotic Signaling

Abstract

Objectives. Our previous study has used RNA-seq technology to show that apoptotic molecules were involved in the myocardial protection of electroacupuncture pretreatment (EAP) on the ischemia/reperfusion (I/R) animal model. Therefore, this study was designed to investigate how EAP protects myocardium against myocardial I/R injury through antiapoptotic mechanism. Methods. By using rats with myocardial I/R, we ligated the left anterior descending artery (LAD) for 30 minutes followed by 4 hr of reperfusion after EAP at the Neiguan (PC6) acupoint for 12 days; we employed arrhythmia scores, serum myocardial enzymes, and cardiac troponin T (cTnT) to evaluate the cardioprotective effect. Heart tissues were harvested for western blot analyses for the expressions of pro- and antiapoptotic signaling molecules. Results. Our preliminary findings showed that EAP increased the survival of the animals along with declined arrhythmia scores and decreased CK, LDH, CK-Mb, and cTnT levels. Further analyses with the heart tissues detected reduced myocardial fiber damage, decreased number of apoptotic cells and the protein expressions of Cyt c and cleaved caspase 3, and the elevated level of Endo G and AIF after EAP intervention. At the same time, the protein expressions of antiapoptotic molecules, including Xiap, BclxL, and Bcl2, were obviously increased. Conclusions. The present study suggested that EAP protected the myocardium from I/R injury at least partially through the activation of endogenous antiapoptotic signaling.

MicroRNA-214-5p protects against myocardial ischemia reperfusion injury through targeting the FAS ligand

“…Interestingly, miR-214 is considered as a target for treatment of I/R diseases due to its protective roles in I/R disease. For instance, the nonselective β-adrenergic receptor antagonist carvedilol or electroacupuncture pretreatment enhanced cardiac function and inhibited cardiomyocyte damage upon simulate I/R injury via enhancing miR-214 expression [8,17]. In the present study, overexpression of miR-214-5p was able to reduce the cardiac cell damage and apoptosis induced by I/R injury in vivo and in vitro.…”

Electroacupuncture pretreatment alleviates myocardial injury through regulating mitochondrial function

“…Patients who have undergone cardiac surgery have shown signi cantly improved heart rates, blood pressure, and rates of recovery after receiving EA stimulation [29]. Recently, researchers found that EA pre-treatment improved the survival rate of rats with myocardial ischemia-reperfusion injury with reduced apoptosis and expressions of Cyt c and cleaved caspase 3 [30,31]. EA regulated the activation of NLRP3, polarization of macrophages, declined arrhythmia scores, improving cardiac function [18,31].…”

“…Recently, researchers found that EA pre-treatment improved the survival rate of rats with myocardial ischemia-reperfusion injury with reduced apoptosis and expressions of Cyt c and cleaved caspase 3 [30,31]. EA regulated the activation of NLRP3, polarization of macrophages, declined arrhythmia scores, improving cardiac function [18,31]. EA played a role of antiarrhythmia through reducing ventricular tachycardia and ventricular, and related to concentration of calcium in the cytoplasm [32,33].…”

Advances in Research on the circRNA‐miRNA‐mRNA Network in Coronary Heart Disease Treated with Traditional Chinese Medicine

“…Ginsenoside Rg1 upregulates the expression of eNOS by targeting miR-214, which is beneficial for promoting angiogenesis [68]. Electroacupuncture preconditioning can upregulate the expression of miR-214 and inhibit the increase in Ca 2+ , sodium/calcium exchanger 1 (NCX1), BCL2-like 11 (BIM), calmodulin-dependent protein kinase IIδ (CaMKIIδ), cyclophilin D (CypD), and other related proteins that have accumulated in hypoxia injury in H9c2 myocardial cells, and play a protective role in ischemia/reperfusion (I/R) [69]. e Fuzheng Huayu capsule has the effect of alleviating myocardial fibrosis after MI in rats.…”