Focal adhesion kinase (FAK) is the key signaling molecule in integrin signal pathway. The activated FAK is closely related to the numerous fibrosis diseases, and plays an important role in the occurrence and development of liver fibrosis. However, the dynamic expressions of FAK during liver fibrogenesis and its reversal are

unknown. Methods: To investigate the expressions of FAK in fibrogenesis and reversal of rat fibrogenic liver tissues and its relation with the hepatic stellate cells in vivo.Methods: Wistar rats were randomly divided into the following groups: model group (received 40% CCl4, n = 24), reversal group (5 weeks’ normal feeding based on received 40% CCl4, n = 24) and control group. H&E staining, MT staining and Sirius red staining were used to determine histopathology changes. Enzalutamide mw The expression of FAK in liver tissues was measured by immunofluorescence staining, real-time fluorescence quantitative PCR (real-time PCR) and western blot. The co-expression between FAK and α-SMA mTOR inhibitor were observed by confocal laser scanning microscopy. Results: The continuous CCl4 injection led to hepatic

cells swelled, and appeared fatty degeneration, necrosis and regeneration. The fibrosis were spread from the vascular smooth muscle cells to portal area and damaged hepatic cells, the latter appeared fatty degeneration, necrosis and regeneration, the enlargened fibrosis area in model group. After the CCl4 injection stop, with spontaneous reverse time extension, the fibrosis tissues turned to be decreased, while the other histopathological changes gradually turned to be normal, especially for the hepatic cells. The protein expressions of α-SMA and FAK were significantly Calpain increased in model group than

that in the control group, and were lowered in reversal group than that at 5 wk in model group (P < 0.01). The expression of FAK mRNA was enhanced during the progressive liver fibrosis and declined during its reversal. The activated HSCs expressing FAK accounted for an increased percentage of total activated HSCs in model group compared with control group (P < 0.01), and for a decreased percentage of total activated HSCs in reversal group (P < 0.01). Co-expression of the areas was mainly concentrated in the fibrous septa, portal area and the proliferation of bile duct cells. There were also significant positive correlations between FAK expression and the percentage of FAK-positive activated HSCs. Conclusion: These data supported that FAK was increased in both liver tissues and HSCs in vivo of rats with hepatic fibrosis, and was decreased in reversal of liver fibrosis. The dynamic expression of FAK in rat liver tissues had a significant positive correlation with the activation and proliferation of HSCs in vivo. Key Word(s): 1. FAK; 2. liver fibrosis; 3.