Hesperidin promotes lysosomal biogenesis in chronically ethanol-induced cardiotoxicity in rats: A proposed mechanisms of protection.

Alcohol consumption is a major global risk factor for mortality and morbidity. We aimed to delineate the mechanisms underlying the potential ameliorative effects of hesperidin against chronically ethanol-induced cardiotoxicity. Sixty male albino rats were divided into normal control group, hesperidin-treated control group, untreated alcoholic group, and hesperidin-treated alcoholic group. Transcription factor-EB (TFEB) expression levels were estimated using real-time reverse transcription-polymerase chain reaction. Peroxisome proliferator-activated receptor γ coactivator 1-α (PGC1-α), macrophage inflammatory protein-1 α, poly-(ADP-ribose)-polymerase-1 (PARP-1) activity, and tenascin C levels in cardiac tissues were estimated by enzyme-linked immunosorbent assay; while tissue malondialdehyde and total antioxidant capacity were evaluated spectrophotometrically. Our data portrayed promoting lysosomal biogenesis, as judged by upregulation of TFEB expression and its target PGC1-α, as well as decreased PARP-1 activity and offsetting inflammation, oxidative stress, and tissue injury as the principal culprits mediating the cardioprotective effect of hesperidin in alcohol-induced cardiotoxicity. In conclusion, hesperidin can be used as a cardioprotective agent in chronically ethanol-induced cardiotoxicity.