Nrf2 signalling pathway and autophagy impact on the preventive effect of green tea extract against alcohol-induced liver injury
| Autor: | Xue-Qin Yang, Jun-Rong Du, Yu-Pei Zhang, Dong-Ke Yu, Heng-Yi Xiao |
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| Rok vydání: | 2021 |
| Předmět: |
Antioxidant
NF-E2-Related Factor 2 medicine.medical_treatment Autophagy-Related Proteins Pharmaceutical Science Green tea extract Pharmacology medicine.disease_cause Antioxidants Mice 03 medical and health sciences 0302 clinical medicine Autophagy medicine Animals Ethanol metabolism Liver Diseases Alcoholic 030304 developmental biology Liver injury 0303 health sciences Tea Plant Extracts Chemistry Metabolism Lipid Metabolism medicine.disease KEAP1 Oxidative Stress Treatment Outcome 030220 oncology & carcinogenesis Beclin-1 Oxidative stress Signal Transduction |
| Zdroj: | Journal of Pharmacy and Pharmacology. 73:986-995 |
| ISSN: | 2042-7158 0022-3573 |
| Popis: | Objectives To explore the potential molecular mechanism underlying the effect of green tea extract (TE), rich in tea polyphenols (TPs), on improving alcohol-induced liver injury. Methods Mice were intragastrically treated with 50% (v/v) alcohol administration (15 ml/kg BW) with or without three doses of TE (50, 120 and 300 mg TPs/kg BW) daily for 4 weeks, and biological changes were tested. Key findings The TE improved the functional and histological situations in the liver of the mice accepted alcohol administration, including enzymes for alcohol metabolism, oxidative stress and lipid accumulation. Interestingly, the TE increased the nuclear translocation of nuclear factor erythroid-2-related factor 2 (Nrf2), with the decreasing expression of kelch-like ECH-associated protein 1 (Keap1), indicating the association between the effect of TE with Nrf2-mediated antioxidant signalling. Moreover, the TE restored the activity of autophagy, showing as lifted Beclin-1 expression, LC3B-II/LC3B-I ratio, and decreased p62 expression. Importantly, all these effects were dose-dependent. Conclusions These findings provide a new notion for the first time that the TE preventing against alcohol-induced liver injury is closely related to accelerated metabolism of alcohol and relieved oxidative stress, which is associated with Nrf2 signalling activation and autophagy restoration, thus the reduction of lipid accumulation in liver. |
| Databáze: | OpenAIRE |
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