No abstract

No abstract

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.

No abstract

Background One of the most common hepatic disorders is nonalcoholic fatty-liver disease. The best model used for nonalcoholic fatty-liver disease is the monosodium glutamate (MSG)-induced obesity. MSG is a common flavor enhancer used in different food products. Vitamin-D deficiency increased risks of obesity and nonalcoholic fatty-liver disease. However, much is still unknown about the link between vitamin D and nonalcoholic fatty-liver disease in obesity. Aim The aim was to investigate the effect of vitamin D on MSG-induced obesity and nonalcoholic fatty-liver disease in rats. Materials and methods Forty adult male albino rats were divided into four equal groups: control group, vitamin-D-treated group, MSG-treated group, MSG, and vitamin-D-treated group, at the end of the experimental period, blood samples were taken. Also, livers were dissected for histopathology. Results Vitamin D+MSG significantly decreased the body weight, serum levels of glucose, insulin and homeostasis model assessment-estimated insulin resistance, triglycerides, tumor necrosis factor-alpha, aspartate aminotransferase, alanine aminotransferase, and the liver malondialdehyde, while increased the liver glutathione levels and improved the liver histological findings compared with MSG group. Conclusion Vitamin D has a hepatoprotective effect on the MSG-induced obesity and nonalcoholic fatty-liver disease.