我们前期研究发现：HBx蛋白诱导肝细胞表达促炎症细胞因子IL-32，IL-32在肝纤维化组织高表达，其表达水平与肝纤维化分期正相关，然而IL-32在肝纤维化形成中的机制仍不明确。肝星状细胞（HSC）活化在肝炎到肝纤维化进程中起重要作用。HSC表达丰富的Intergrins及FAK，不同的Integrins与其配体结合调节Integrins/FAK通路，影响HSC活化。IL-32可结合αVβ3、αVβ6 Integrins及 FAK，因此我们推测IL-32可能通过调节Integrins/FAK通路活化HSC而促纤维化。本课题利用细胞模型和肝组织标本研究IL-32对HSC活化增殖迁移及HSC Integrins表达的影响，探讨IL-32调控Integrins/FAK通路的机制，阐明IL-32/Integrins/FAK通路在肝纤维化形成中的作用，为以此为靶点的早期逆转肝纤维化治疗提供理论依据。

In our previous study, we found that HBx could induce the expression of IL-32 (a proinflammatory cytokine) by hepatocyte, and IL-32 expression was increased in liver tissue of fibrosis. Furthermore, the level of hepatic IL-32 expression was positively correlated with the stage of liver fibrosis. But the molecular mechanism of IL-32 in the formulation of liver fibrosis is not clear. Hepatic stellate cell (HSC) plays an important role in the progression from hepatitis to liver fibrosis. FAK and many Integrins are expressed by HSC. After different Integrins are engaged by different ligands, Integrins/FAK signaling pathway is regulated and followed with the activation of HSC. It is found that IL-32 could bind to FAK and Integrins such as αVβ3, αVβ6, so we suggest that IL-32 could activate HSC and then promote the formulation of liver fibrosis by regulation of Integrins/FAK signaling pathway. In the present study, cell model and liver tissue are utilized to research the effect of IL-32 on activation, proliferation and migration of HSC. Then the effect of IL-32 on Integrins expression by HSC is investigated. Subsequently, the mechanism of IL-32 in regulating Integrins/FAK signaling pathway is defined. Finally, the effect of IL-32/Integrins/FAK signaling pathway on the formulation of liver fibrosis is clarified. The aim of the study is to provide theoretical basis for regarding IL-32/Integrins/FAK signaling pathway as treatment target for early reversal of liver fibrosis.