细胞衰老与肝纤维化的形成密切相关，活化的肝星状细胞（HSCs）衰老能限制肝纤维化发展。白介素-10（IL-10）是一多效性炎症抑制因子及对肝纤维化产生具有调节作用。我们前期研究证实IL-10可抑制HSCs活化、增殖而拮抗肝纤维形成，伴随纤维沉积区细胞衰老增多，但IL-10是否能直接促进活化HSCs衰老，未见报道。课题拟通过IL-10干预对不同活化状态的原代HSCs及纤维化大鼠，细胞化学与流式细胞观察HSCs衰老与细胞周期改变，定量PCR与免疫印迹检测JAK1-STAT3-SOCS3信号与衰老指标的变化，评估IL-10对HSCs衰老及信号通路的影响；采用RNA干扰沉默SOCS3基因与特异性抑制剂阻断STAT3信号，再次评估IL-10对HSCs衰老的影响。课题有助于阐明IL-10抗纤维化机制，为IL-10临床抗纤维化治疗提供一种新视角和实验数据。

Senescence is associated with the development of liver fibrosis. Senescence of activated Hepatic stellate cells (HSCs) limits liver fibrosis. Interleukin-10 (IL-10) is a pleiotropic cytokine that downregulates the proinflammatory response and has a modulatory effect on hepatic fibrogenesis. Our previous study had reported that IL-10 attenuates liver fibrosis in rats by inhibiting the activation and proliferation of HSCs, which associated with the increase of cells senescence number in the area of fibrogenesis. However, little is known regarding the effect of IL-10 on senescence of activated HSCs. In this study, the primary HSCs in different state of activation and the fibrotic rats were treated with IL-10，the change of senescence and cell cycle of HSCs were assessed by immunocytochemistry and flow cytometry analysis. Real-Time PCR and Western Blot analysis were used to detect the gene and protein expression of JAK1-STAT3-SOCS3 signal pathway and senescence of HSCs. This study was to investigate the effluence of IL-10 on the senescence of HSCs and its signal pathway, and then to assess the effect of shRNA interference targeting SOCS3 gene and a specific inhibitor for STAT3 on senescence of primary HSCs treated with IL-10.This study is designed to give a interpretation for the anti-fibrotic mechanism of IL-10 and will provide a new insight and experience data for anti-fibrotic therapy of IL-10.