2018PubMedRequires access

[The protective effect of tea polyphenols on chronic alcoholic liver injury in rats].

Yong Zhang, Miaomiao Li, Tianmiao Hua, Qingyan Sun

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Abstract

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: <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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What this paper is about

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: <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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Available abstract

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: <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.

Key concepts: Liver injury, Glutathione peroxidase, Malondialdehyde, Chemistry, Lipid peroxidation, CD36, Internal medicine, Superoxide dismutase

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