Effects of Epigallocatechin-3-gallate on Nonalcoholic Fatty Liver Disease in Mice
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Abstract:
The protective effects of epigallocatechin gallate (EGCG) on nonalcoholic fatty liver disease (NAFLD) in mice were investigated. The NAFLD ApoE-/- mice model was established by feeding high fat food. Then, the effects of EGCG on glucose and lipid metabolism, fatty acid oxidation, oxidative stress level, liver tissue structure and the gene expressions of AMPK/SIRT1/SREBP-1c/PPARγ signaling pathway in NAFLD mice were analyzed. The results indicated that after EGCG treatment, the pathological changes of liver tissue were evidently ameliorated; compared with the model group, the body weight, liver mass and liver mass index of mice were significantly reduced to 110.98%, 115.01%, 115.64%, 136.48% and 104.20%, 118.70% respectively (p<0.01, respectively). The levels of glucose and lipid metabolism, fatty acid oxidation and oxidative stress in blood and liver tissues were markedly improved by 11.85%~86.06% compared with model group (p<0.05 or p<0.01, respectively). Further study indicated that the AMPKα, SIRT1 mRNA and p-AMPKα, SIRT1 protein expressions in liver tissue were obviously elevated by 13.21%~75.82%. In contrast, the FASN、ACC-1、SREBP-1c、SCD-1、PPARγ mRNA and FASN、p-ACC-1、p-SREBP-1c、SCD-1、PPARγ protein expressions in liver tissue were dramatically reduced by 19.59%~92.07%, the p-AMPKα/AMPKα、p-ACC-1/ACC-1 and p-SREBP-1c/SREBP-1c ratios significantly ameliorated by 39.20%~93.07% compared with model group (p<0.05 or p<0.01, respectively). The results demonstrated that EGCG could ameliorate glucose and lipid metabolism, fatty acid oxidation and oxidative stress in NAFLD mice by regulating there lated gene expressions of AMPK/SIRT1/SREBP-1c/PPARγ signaling pathway.