Moxibustion Protects Against Oxidative Stress-Induced Cardiomyocyte Apoptosis by Modulating SIRT1/p53/Bax Signaling in H9C2 Cells

Abstract

Objective: This study aimed to systematically analyze the molecular mechanism by which oxidative stress-regulated SIRT1/p53/Bax signaling inhibits apoptosis in H9C2 cardiomyocytes and to elucidate the potential therapeutic targets of traditional Chinese medicine moxibustion therapy for preventing exercise-induced cardiac myocardial injury through the regulation of this pathway. Methods: An oxidative stress injury model was established in H9C2 cardiomyocytes using oxygen–glucose deprivation (OGD). The cells were organized into seven distinct groups: normal control (N), normal + blank serum (NC), normal + model serum (NMD), normal + moxibustion serum (NMOX), OGD-treated (OGD), OGD + blank serum (OGDC), and OGD + moxibustion serum (OGDM). Lactate dehydrogenase (LDH) release was measured by enzyme-linked immunosorbent assay (ELISA), apoptosis was assessed using TUNEL assays, and protein expression was analyzed by immunocytochemistry and Western blotting. Results: Compared with the N group, the OGD group exhibited significantly increased LDH release (P < 0.01); an increased apoptosis rate (P < 0.01); upregulated expression of p53, acetyl-p53, Bax, Cyt-c, caspase-9, cleaved caspase-9, caspase-3, and cleaved caspase-3 (all P < 0.01); and decreased levels of SIRT1 and Bcl-2 (both P < 0.01). In contrast, the OGDM group exhibited opposite trends, with reduced LDH release (P < 0.01), a lower apoptosis rate (P < 0.01), downregulated expression of apoptotic proteins (all P < 0.01), and increased expression of SIRT1 and Bcl-2 (both P < 0.01). Conclusion: Moxibustion has potential protective effects against exercise-induced myocardial injury through the modulation of the SIRT1/p53/Bax pathway to inhibit apoptosis in heart cells.