Frontiers in veterinary science · 2026
The potential protective mechanisms of melatonin on alcoholic fatty liver disease based on the animal study.
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Wu Haixin, Zhu Tianqi, Guo Fei, Zhang Lu, Wang Bingyuan, Liu Guoshi
Аннотация
INTRODUCTION: Alcoholic fatty liver disease (AFLD) is one of the most common alcohol-related liver disorders and is characterized by hepatic lipid accumulation, oxidative stress, and hepatocyte injury. Melatonin (MT), a potent antioxidant and free-radical scavenger, has been reported to exert hepatoprotective effects; however, its protective mechanisms against chronic alcohol-induced AFLD remain incompletely understood.
METHODS: A mouse model of AFLD was established by chronic alcohol administration in male ICR mice. Animals were randomly assigned to a control group, an alcohol (ALC) group, and three MT treatment groups receiving 0.0025, 0.5, or 5 mg/kg/day MT. Body weight, serum AST/ALT ratio, organ coefficients, liver histopathology, hepatic lipid accumulation, malondialdehyde (MDA) levels, and the expression of oxidative stress- and apoptosis-related genes were evaluated.
RESULTS: Chronic alcohol consumption significantly reduced body weight gain, increased the serum AST/ALT ratio, induced hepatic steatosis, elevated hepatic total cholesterol (TC), triglyceride (TG), and MDA levels, and altered the expression of genes associated with oxidative stress and apoptosis. MT supplementation attenuated alcohol-induced liver injury in a dose-dependent manner. MT significantly reduced hepatic TC, TG, and MDA levels, improved liver histopathology, and suppressed alcohol-induced upregulation of Cyp2e1. In addition, MT partially modulated the expression of apoptosis-related genes, suggesting a protective role against hepatocyte damage.
DISCUSSION: Melatonin effectively alleviates chronic alcohol-induced AFLD by reducing hepatic lipid accumulation, oxidative stress, and apoptosis-related alterations. These findings provide mechanistic evidence supporting the potential application of melatonin as a complementary strategy for the prevention and management of AFLD.
METHODS: A mouse model of AFLD was established by chronic alcohol administration in male ICR mice. Animals were randomly assigned to a control group, an alcohol (ALC) group, and three MT treatment groups receiving 0.0025, 0.5, or 5 mg/kg/day MT. Body weight, serum AST/ALT ratio, organ coefficients, liver histopathology, hepatic lipid accumulation, malondialdehyde (MDA) levels, and the expression of oxidative stress- and apoptosis-related genes were evaluated.
RESULTS: Chronic alcohol consumption significantly reduced body weight gain, increased the serum AST/ALT ratio, induced hepatic steatosis, elevated hepatic total cholesterol (TC), triglyceride (TG), and MDA levels, and altered the expression of genes associated with oxidative stress and apoptosis. MT supplementation attenuated alcohol-induced liver injury in a dose-dependent manner. MT significantly reduced hepatic TC, TG, and MDA levels, improved liver histopathology, and suppressed alcohol-induced upregulation of Cyp2e1. In addition, MT partially modulated the expression of apoptosis-related genes, suggesting a protective role against hepatocyte damage.
DISCUSSION: Melatonin effectively alleviates chronic alcohol-induced AFLD by reducing hepatic lipid accumulation, oxidative stress, and apoptosis-related alterations. These findings provide mechanistic evidence supporting the potential application of melatonin as a complementary strategy for the prevention and management of AFLD.