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目的研究干扰素(IFN)α1b治疗肝纤维化的作用机制。方法将体外培养大鼠贮脂细胞分为对照组、肿瘤坏死因子(TNF)α组、IFNα1b组和TNFα+IFNα1b组,应用免疫组织化学和透射电镜观察各组贮脂细胞形态学改变及过氧化物酶增生激活受体(PPAR)α的表达。结果肿瘤坏死因子α在50U/ml浓度时,贮脂细胞吸光度值(A)为0.401±0.27,增殖率为450.3±309.1(P<0.01);透射电镜显示IFNα1b组细胞形态改变符合凋亡的早期形态特征;免疫组织化学观察到贮脂细胞中PPARα的阳性单位值(PU)为24.69±4.88,较对照组和其余两组明显增高,差异有统计学意义(P<0.01)。结论IFNα1b对肿瘤坏死因子α促进贮脂细胞增殖激活的过程有抑制作用,作用机制可能是通过诱导肝脏贮脂细胞凋亡而产生。
Objective To study the mechanism of interferon (IFN) α1b in the treatment of hepatic fibrosis. Methods The adipocytes were divided into control group, tumor necrosis factor (TNF) α group, IFNα1b group and TNFα + IFNα1b group. Immunohistochemistry and transmission electron microscope were used to observe the morphological changes and peroxidation The expression of PPARα. Results At 50 U / ml, the absorbency value (A) was 0.401 ± 0.27 and the proliferation rate was 450.3 ± 309.1 (P <0.01). The morphological changes of IFNα1b group were in accordance with the early stage of apoptosis Immunohistochemistry showed that the positive unit value (PU) of PPARα in storage fat cells was 24.69 ± 4.88, which was significantly higher than that in control group and the other two groups (P <0.01). Conclusion IFNα1b can inhibit tumor necrosis factor-α (TNF-α) -mediated proliferation and activation of storage-bearing cells. The mechanism may be through inducing the apoptosis of liver fat-storage cells.