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Inflammation, oxidative stress (OS), and obesity are documented to play key roles in the pathogenesis of cardiovascular diseases (CVDs). Accordingly, tumor necrosis factor-α (TNF-α) and hydrogen peroxide (H2 O2 ), as a main innate immunity pro-inflammatory cytokine and a main free radical, respectively, are the main risk factors for CVDs. The present study aimed to evaluate the effects of OS, regular aerobic exercise (RAE), and vitamin D3 (VD3) on the expression of TNF-α in the myocardial cells in a rat model. Methods: In this experimental study, 48 male Wistar rats were divided into 8 groups (6 in each group) including healthy controls, sham (injected with dimethyl sulfoxide [DMSO] + saline), H2 O2 (either 1 or 2 mmol/kg), H2 O2 (1 mmol/kg) + VD3, H2 O2 (2 mmol/kg) + VD3, H2O2 (1 mmol/kg) + RAE, and H2 O2 (2 mmol/kg) + RAE. TNF-α level of myocardial cells was evaluated after 8 weeks using the ELISA technique. Results: The results of the study demonstrated that exposure to 2 mmol/kg of H2 O2 significantly increased TNF-α level of myocardial cells compared to the rats which were exposed to one mmol/ kg H2 O2 (P=0.039). Furthermore, RAE (P=0.040), and the combination of RAE+VD3 (P=0.049) significantly reduced the expression of myocardial TNF-α. Conclusion: In general, VD3 and RAE were found to suppress TNF-α expression induced by H2 O2 in the rat myocardium. Therefore, they can be considered as potential therapeutic interventions for reducing OS-induced inflammation in the damaged myocardial cells.

Regular Aerobic Exercise and Vitamin D3 Supplementation-Reduced Anthropometric Measures and the Hydrogen Peroxide-Induced Expression of TNF-α in Rats