Liwei Wu 1 , Qinghui Zhang 2 , Wenhui Mo 3 , Jiao Feng 1 , Sainan Li 1 , Jingjing Li 1 , Tong Liu 1 , Shizan Xu 4 , Wenwen Wang 1 , Xiya Lu 1 , Qiang Yu 4 , Kan Chen 1 , Yujing Xia 1 , Jie Lu 1 , Ling Xu 5 , Yingqun Zhou 1 , Xiaoming Fan , 6 , Chuanyong Guo , 1
24 August 2017
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 (CCl 4) 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 CCl 4 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-β1/Smads signaling pathway and activating the PI3K/Akt signaling pathway to inhibit autophagy in BDL- or CCl 4- induced liver fibrosis. Quercetin prevented hepatic fibrosis by attenuating hepatic stellate cell activation and reducing autophagy through regulating crosstalk between the TGF-β1/Smads and PI3K/Akt pathways.