Abstract

The aim of this study was to investigate the hepatoprotective effects of resveratrol in alcoholic liver disease (ALD). Alcohol was administered to healthy female rats starting from 6% (v/v) and gradually increased to 20% (v/v) by the fifth week. After 16 weeks of intervention, liver enzymes (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]) were analyzed using a chemistry analyzer, while hepatic antioxidant enzymes, oxidative stress markers, and caspase 3 activity were assessed using ELISA kits. Furthermore, hepatic CYP2E1 protein levels and mRNA levels of antioxidant and inflammation-related genes were determined using western blotting and RT-PCR, respectively. The results showed that resveratrol significantly attenuated alcohol-induced elevation of liver enzymes and improved hepatic antioxidant enzymes. Resveratrol also attenuated alcohol-induced CYP2E1 increase, oxidative stress, and apoptosis (caspase 3 activity). Moreover, genes associated with oxidative stress and inflammation were regulated by resveratrol supplementation. Taken together, the results suggested that resveratrol alleviated ALD through regulation of oxidative stress, apoptosis, and inflammation, which was mediated at the transcriptional level. The data suggests that resveratrol is a promising natural therapeutic agent against chronic ALD.

Highlights

  • Alcoholic liver disease (ALD) often results from binge overconsumption of alcohol

  • ALD encompasses fatty liver, alcoholic hepatitis, and chronic hepatitis with liver fibrosis, which are caused by the toxic effects of the byproducts of alcohol metabolism [4, 5]

  • Rat superoxide dismutase (SOD) and catalase (CAT) enzyme-linked immunosorbent assay (ELISA) kits were purchased from Cell Biolabs

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Summary

Introduction

Alcoholic liver disease (ALD) often results from binge overconsumption of alcohol. Epidemiological investigations have shown that, in the developed countries of Europe and America, liver diseases account for a significant cause of morbidity and mortality [1, 2]. ALD is becoming a global problem with increasing cases in the developing countries [3]. ALD encompasses fatty liver, alcoholic hepatitis, and chronic hepatitis with liver fibrosis, which are caused by the toxic effects of the byproducts of alcohol metabolism [4, 5]. Clinical testing has demonstrated that ALD patients normally have protein and/or combined protein-calorie malnutrition [6]. Risk factors for the development of ALD, including excessive alcohol intake, high fat diet, and calorie malnutrition, have been adopted in the rat model

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