Cardioprotective role of metformin against sodium arsenite-induced oxidative stress, inflammation, and apoptosis.

Arsenic is a universal component and a notable natural poison. Its exposure to people occurs primarily through natural, therapeutic, and occupational sources. This investigation intended to discover the defensive impact of metformin (100 and 150 mg/kg body weight) against sodium arsenite (SA)-induced cardiotoxicity in experimental animals. The study was conducted on Sprague Dawley rats (n = 50), which were separated into five different groups as follows: control, met-150, SA, SA + met-100, and SA + met-150. The results demonstrated that SA caused a significant increase in the level of malondialdehyde and also reduced activities of antioxidative enzyme. SA similarly increased inflammatory reactions by increasing the level of interleukin-6, tumor necrosis factor-α, and interleukin-1β. In addition, SA provoked the apoptosis by expanding the p53 and Bax levels, terminal deoxynucleotidyl transferase dUTP nick end labeling, and expression of caspase-3. SA altered the histological integrity of cardiac tissue and 8-hydroxy-2'-deoxyguanosine expression. In conclusion, metformin significantly reduced oxidative stress, inflammatory reaction, and apoptotic pathway. The present investigation showed that metformin has a cardioprotective impact because of its protective role against oxidation, inflammation, and apoptosis.