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Abstract

Objective: Clinical studies have shown that moxibustion at CV8 can prevent pathological myocardial injury and improve heart function; however, the underlying mechanisms remain unclear. This study explored how moxibustion at CV8 prevents and treats exercise-induced ventricular arrhythmia by inhibiting cardiomyocyte apoptosis via the SIRT1/p53/Bax pathway. Methods: A 12-week treadmill exercise regimen was implemented to develop a rat model of exercise-induced ventricular arrhythmia. The impact of moxibustion at CV8 on this condition was evaluated by analyzing serum biomarkers, myocardial cell mitochondria, and tissue-related indicators using ELISA, colorimetric assays, Western blotting, immunohistochemistry, and HE and TUNEL staining. Results: Moxibustion at CV8 effectively alleviated myocardial injury, improved pathological electrocardiograms, and lowered the serum levels of BNP, CK-MB, cTnI, and cTnT. It also reduced myocardial tissue levels of p53, acetyl-p53, Cyt-c, Bax, caspase-9, cleaved caspase-9, caspase-3, and cleaved caspase-3 while increasing the activity of myocardial mitochondria I–IV and the expression of SIRT1 and Bcl-2, thereby inhibiting myocardial cell apoptosis. Conclusions: Moxibustion at CV8 inhibits myocardial cell apoptosis and prevents exercise-induced ventricular arrhythmia by regulating the SIRT1/p53/Bax pathway.

Keywords

moxibustion CV8 sports-induced ventricular arrhythmia apoptosis SIRT1 p53

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Efficacy of Moxibustion at CV8 on Exercise-Induced Ventricular Arrhythmia: Inhibition of Cardiomyocyte Apoptosis via the SIRT1/p53/Bax Pathway

Abstract

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