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Cardioprotective effect of electroacupuncture in cardiopulmonary bypass through apelin/APJ signaling

Wang, Ke, Ju, Ziyong, Chen, Changle, Fan, Shendong, Pei, Lijuan, Feng, Chenchen, Wang, Fengjiao, Cui, Huashun, Zhou, Jia
Life sciences 2020 v.242 pp. 117208
apoptosis, cardioprotective effect, caspase-3, electroacupuncture, fluorescent antibody technique, glutathione, heart, inflammation, interleukin-1beta, lactate dehydrogenase, mitogen-activated protein kinase, myeloperoxidase, nucleotidyltransferases, oxidation, oxidative stress, patients, signal transduction, staining, troponin I, tumor necrosis factor-alpha
AimAcupuncture, particularly electroacupuncture (EA), can improve the clinical outcomes of cardiopulmonary bypass (CPB) patients; however, the mechanisms remain unclear. This study aimed to examine the effects of EA pre-treatment on myocardial injury after CPB and investigate its potential mechanisms.Male Sprague-Dawley rats were subjected to CPB and divided into Control (sham-operated), CPB, and EA (CPB + EA) groups. In the EA group, rats were treated with EA at the “PC6” acupoint for 30 min before being subjected to CPB. At 0.5, 1, and 2 h after CPB, the expression levels of plasma cardiac troponin I (cTnI) and lactate dehydrogenase (LDH), and myeloperoxidase (MPO) activity, TNFα, IL-1β, reduced glutathione (GSH), oxidized glutathione (GSSH), and the ratio of GSH/GSSH in the myocardial tissue were measured. Apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) staining. The expression of cleaved caspase-3 was detected by immunofluorescence. The expression of apelin, APJ, AKT, p-Akt, ERK1/2, and p-ERK1/2 was determined using western blotting.Decreased myocardial injury marker levels, myocardial apoptosis, oxidative stress, and the inflammatory response were found in the EA group compared with the CPB group. The expression levels of apelin, APJ, and p-Akt/AKT were increased in the EA group, and the p-ERK1/2/ERK1/2 level was decreased.This study showed that EA pre-treatment can protect the heart from damage following CPB, which might be mainly mediated by restoring the apelin/APJ signaling pathway.