Diminazine protects against cardiac aging through the improvement of mitophagy and apoptosis in aging rats induced by D-galactose

BackgroundMitochondrial dysfunction is a main feature of the aged heart. However, there is still no effective treatment against cardiac aging. Diminazine (DIZE) is an anti-infective agent for animals. It is effective against cardiac disorders. The present study aimed to investigate the effects of DIZE on age-related cardiac dysfunction.Methods and resultsWistar rats were randomly divided into four groups, with eight rats per group: control rats (CONT), control rats treated with DIZE (CONT + DIZE), aged rats induced by D-galactose (D-GAL), aged rats treated with DIZE (D-GAL + DIZE). Rats received intraperitoneal (IP) injection of D-GAL at 150 mg/kg daily for 8 weeks to induce aging. The aging animals in the D-GAL + DIZE group were treated with subcutaneous injection of DIZE at 15 mg/kg daily for 8 weeks. Heart tissues were harvested to assay molecular parameters. Our results exhibited cardiac hypertrophy and a significant increase in the expression of cardiac BCL2-associated X (Bax) along with a significant decrease in the expression of cardiac Mitofusin 2 (Mfn2), Phosphatase, and tensin homolog (PTEN)-induced putative kinase 1 (PINK1), Dynamin-related protein 1 (Drp1), and B-cell lymphoma 2 (Bcl2) in the aged rats compared with the control animals. DIZE treatment improved cardiac hypertrophy and the expression of genes.ConclusionsOverall, DIZE treatment significantly reversed the downregulation of PINK1, Mfn2, and Drp1. Moreover, DIZE significantly inhibited apoptosis though improving the gene expression of Bax and Bcl-2 in the heart. DIZE is effective in reducing cardiac hypertrophy induced aging through regulating mitochondrial dynamics, mitophagy and apoptosis.