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Quercetin prevents hepatic fibrosis by inhibiting hepatic stellate cell activation and reducing autophagy via the TGF-beta 1/Smads and PI3K/Akt pathways

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机构: [1]Tongji Univ, Sch Med, Shanghai Tenth Peoples Hosp, Dept Gastroenterol, Shanghai 200072, Peoples R China [2]Jiangsu Univ, Kunshan Peoples Hosp 1, Dept Clin Lab, Kunshan 215300, Jiangsu, Peoples R China [3]Fudan Univ, Minhang Hosp, Dept Gastroenterol, Shanghai 201100, Peoples R China [4]Nanjing Med Univ, Shanghai Tenth Hosp, Sch Clin Med, Dept Gastroenterol, Shanghai 200072, Peoples R China [5]Shanghai Jiao Tong Univ, Sch Med, Shanghai Tongren Hosp, Dept Gastroenterol, Shanghai 200336, Peoples R China [6]Fudan Univ, Jinshan Hosp, Dept Gastroenterol, Shanghai 201508, Peoples R China
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The aim of this study was to investigate the effect of quercetin on hepatic fibrosis, a characteristic response to acute or chronic liver injury. Mice were randomized to bile duct ligation (BDL) or carbon tetrachloride (CCl4) cirrhosis models. Quercetin (100 mg/kg or 200 mg/kg daily) was administered by gavage for 2 or 4 weeks. Liver tissue and blood samples were collected for histological and molecular analysis. The results of our experiments showed that quercetin reduced BDL or CCl4 liver fibrosis, inhibited extracellular matrix formation, and regulated matrix metallopeptidase (MMP)-9 and tissue inhibitor of metalloproteinase (TIMP)-1. Quercetin attenuated liver damage by suppressing the TGF-beta 1/Smads signaling pathway and activating the PI3K/Akt signaling pathway to inhibit autophagy in BDL or CCl4- induced liver fibrosis. Quercetin prevented hepatic fibrosis by attenuating hepatic stellate cell activation and reducing autophagy through regulating crosstalk between the TGF-beta 1/Smads and PI3K/Akt pathways.

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出版当年[2016]版:
大类 | 2 区 综合性期刊
小类 | 2 区 综合性期刊
最新[2023]版:
大类 | 2 区 综合性期刊
小类 | 2 区 综合性期刊
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出版当年[2015]版:
Q1 MULTIDISCIPLINARY SCIENCES
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Q1 MULTIDISCIPLINARY SCIENCES

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第一作者机构: [1]Tongji Univ, Sch Med, Shanghai Tenth Peoples Hosp, Dept Gastroenterol, Shanghai 200072, Peoples R China
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