Hesperidin promotes lysosomal biogenesis in chronically ethanol-induced cardiotoxicity in rats: A proposed mechanisms of protection
| Autor: | Hanaa H, Gaballah, Heba B, Ghanem, Nahid M, Tahoon, Darin A, Mohamed, Abla M, Ebeid |
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| Rok vydání: | 2018 |
| Předmět: |
Male
Cardiotonic Agents Organelle Biogenesis Ethanol Basic Helix-Loop-Helix Leucine Zipper Transcription Factors Hesperidin Myocardium Poly (ADP-Ribose) Polymerase-1 Heart Tenascin Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha Cardiotoxicity Rats Oxidative Stress Gene Expression Regulation Animals Lysosomes Chemokine CCL3 |
| Zdroj: | Journal of biochemical and molecular toxicology. 33(3) |
| ISSN: | 1099-0461 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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