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

Abstract

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.

Metformin: a novel promising option for fertility preservation during cyclophosphamide-based chemotherapy

“…Accumulated evidence reported that metformin could inhibit tumorigenesis and cancer progression by affecting cancer cell metabolism, promoting apoptosis and decreasing cell proliferation in various cancer cell types, such as in colon ( Sena et al , 2018 ), ovarian ( Zou et al , 2019 ), breast ( Malki and Youssef, 2011 ) and prostate cancer ( Demir et al , 2014 ). However, in our study conflicting results were noted when studying the cell proliferative and anti-apoptotic effects of metformin in the ovarian granulosa cells under the stress of chemotherapeutic agents, which agreed with another murine study, which reported a cardioprotective effect against apoptosis and inflammation during arsenic poisoning ( Wang et al., 2020 ). It is possible that metformin is more likely to exert an anti-apoptotic effect under a preexisted stressful cellular condition.…”

Nephroprotective effects of chlorogenic acid against sodium arsenite‐induced oxidative stress, inflammation, and apoptosis

“…In the present study, As exposure induced significant renal cell apoptosis, as evidenced by the increased expressions of Bax and caspase 3 and the decreased expression of Bcl-2. Wang et al 46 found that As induced cardiac apoptosis in a rat model via the expulsion of cytochrome c from the mitochondria, which enhanced the activity of caspase 3 and, consequently, the proteolytic production of poly (ADP-ribose) polymerase and the destruction of DNA. Mu et al 47 further reported that As stimulates apoptosis by upregulating the expressions of caspase 3, Bax, and p53 in the MA-10 murine Leydig tumor cell line.…”

Metformin Regulates Autophagy to Attenuate Mitochondrial Dysfunction in High Glucose-stimulated H9C2 Cardiomyocytes via the AMPKα/Sirt1/Parkin Signaling Axis

“…Metformin has a variety of myocardial protective functions, such as improving oxidative stress and reducing apoptosis (29,30). To further verify the therapeutic effect of metformin on DCM, we performed an in vitro study and con rmed that metformin can activate mitophagy, reduce the levels of intracellular ROS, improve mitochondrial function, and reduce apoptosis.…”