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Updated: Jan 25, 2026

Histological Analyses of Acute Alcoholic Liver Injury in Zebrafish
Published on: May 25, 2017
[The protective effect of tea polyphenols on chronic alcoholic liver injury in rats]
Yong Zhang1, Miao-Miao Li1, Tian-Miao Hua1
1College of Life Science, Anhui Normal University, Wuhu 241000, China.
Objective:
To investigate the protective effects and potential mechanisms of tea polyphenols intervention on excess alcohol intake induced liver injury in rats. This study established the animal model of chronic liver injury rats induced by alcohol. Our results will provide experimental evidence for the effects of tea polyphenol on chronic alcoholic liver injury.
Methods:
Alcohol-induced liver injury rat models were established, and the tea polyphenols intervention was performed in the meantime. After 8 weeks, rats were anesthetized, and visceral fat and liver samples were separated, weighted and stored. Visceral fat content was evaluated in fat/body weight ratio. Liver lipid accumulation was assessed by liver index and the result of Oil Red O staining. Hepatic superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, total antioxidant capacity assay (T-AOC) and glutathione peroxidase (GSH-Px) activity were detected. And fatty acid translocase (FAT/CD36) protein level in liver was detected.
Results:
Compared with the control group rats, the fat/body weight ratio, SOD/MDA, T-AOC and GSH-Px activity of chronic liver injury rats were decreased significantly (P<0.05,P<0.01). Meanwhile the liver index, FAT/CD36 protein level and lipid deposition in liver of chronic liver injury rats were increased (P<0.01). Compared with chronic liver injury rats, the tea polyphenols intervention increased fat/body weight ratio (P<0.05), and significantly increased SOD/MDA, T-AOC and GSH-Px activity (P<0.01). Meanwhile the tea polyphenols intervention reduced liver index (P<0.01), FAT/CD36 protein level (P<0.01) and lipid deposition in liver.
Conclusions:
Tea polyphenols intervention can improve lipid deposition and oxidative stress in chronic alcoholic liver, which is concurrent with decreased FAT/CD36 protein expression on the hepatocyte membrane.
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