IL-10对TNF-α诱导肝星状细胞激活的抑制作用

摘要

Objective To investigate the inhibition of interleukin-10( IL-10 ) in the activation of human hepatic stellate cells ( HSC ) induced by tumor necrosis factor-a ( TNF-a ). Methods The models of HSC in vitro were established by induction with 10 ng/ml TNF-a stimulation and different concentrations of IL-10 ( 2,10,20 ng/ml ), which were observed at the different time periods( 1 , 2, 24, 48 , 72, 96 h ). The Oil red 0 was used to determine the activation changes of HSC and the ability of fat store. The expressions of a-SMA and MCP-1 in HSC were detected by Western blot and RT-PCR. Results The stimulation of TNF-a could activate HSC into fibroblasts cells, and decrease the fat storage. The expression of a-SMA and MCP-1 were increased with time ( P <0. 05 ) in a certain concentration-dependent manner( P <0. 05 ). With combined usage of IL-10, the levels of a-SMA and MCP-1 had also decreased significantly ( P <0. 05 ), and showed a dose-dependent manner( P < 0. 05 ). Conclusion IL-10 can inhibit TNF-a and prevent the activation of HSC,protect the liver from early inflammation and fibrosis.%目的 探讨白细胞介素-10(IL-10)对肿瘤坏死因子-α(TNF-α)诱导的人肝星状细胞(HSC)激活的抑制作用.方法 使用10 ng/ml TNF-α刺激体外培养的HSC,建立HSC激活模型,给予HSC激活模型不同浓度IL-10(2、10、20 ng/ml)作用不同时间(1、2、24、48、72、96 h)后,油红O染色观察细胞脂肪含量,分别用Western blot和RT-PCR检测α-平滑肌肌动蛋白(α-SMA) 和单核细胞趋化蛋白-1(MCP-1)表达水平.结果 TNF-α刺激后,HSC脂肪含量显著减少,α-SMA和MCP-1表达量水平均随时间延长而升高(P<0.05).联合使用IL-10,α-SMA水平显著下降(P<0.05),且具有浓度依赖性(P<0.05),MCP-1水平亦下降(P<0.05).结论 IL-10可以抑制由TNF-α诱导的HSC激活,在肝脏早期炎症和肝纤维化进程中起保护作用.