Protective Effect of Betanin Inhibits Inflammation and Apoptosis through Modulate PTEN/AKT Signaling Pathway in Doxorubicin-Induced Cardiotoxicity Rats

Doxorubicin (DOX) is an effective anti-neoplastic mediator; however, the usage is limited owing to its cardiomyopathy. Betanin is an active radical scavenger widely used in the regulation of cerebrovascular blood supply. The present work was focused on investigating the effect of betanin (Pre-treated) in rats with cardiomyopathy induced by DOX. Cardiotoxicity was induced by IP injection of DOX (15 mg/kg) for two weeks in the rat. DOX treated rats showed an increase in lipid peroxidation (TBARS) and decreased antioxidants status (SOD, CAT, GST, GSH, GST, GR, and GPx). We observed irregular pathological structures in DOX-induced rats. The DOX treatment significant increase the myocardium biomarkers such as Ct-I, BNP, CK-MB in serum. Significantly enhanced activity of pro-inflammatory cytokines in DOX treated rats. Betanin treated rats show increased antioxidants, reduced cardiac damage biomarkers, and suppressed inflammatory cytokines in DOX-induced rats. Furthermore, a DOX-induced rat shows increased PTEN, PI3K, and decreased p-AKT, thereby enhancing pro-apoptotic protein Bax, Bad, Caspase 3 expression resulting in induced cell apoptosis. Whereas betanin treatment significantly down in the activation PTEN/AKT and pro-apoptotic protein, enhance Bcl-2 expression in DOX-mediated rats. The overall finding shows that betanin inhibits inflammation and cell apoptosis by modulating PTEN/AKT signaling in the DOX-induced rat.