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机构地区:[1]中山大学附属第一医院肝胆外科,广州510080 [2]广州市荔湾区医院外科
出 处:《中华实验外科杂志》2005年第3期300-301,i006,共3页Chinese Journal of Experimental Surgery
摘 要: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 alpha1b in curing hepatic fibrosis.Methods The rat fat-storing cells cultured in vitro were divided into control group,tumor necrosis factorα group,interferon alpha1b group and tumor necrosis factorα+ interferon alpha1b group.The morphologic changes of fat-storing cells were observed under transmission electron microscopy and the expression of peroxisome proliferator-activated receptor alpha detected by immunohistochemistry.Results When the concentration of tumor necrosis factor alpha was 50 U/ml,the absorbance of fat-storing cell was 0.401±0.27,and rate of proliferation was 450.3±309.1 (P<0.01).The morphologic change of the fat-storing cells in interferon alpha1b group had the phenomenon of apoptosis under transmission electron microscopy.The positive unit of peroxisome proliferator-activated receptor alpha in fat-storing cells was 24.69±4.88,significant higher than in other three groups (P<0.01).Conclusion Interferon alpha1b can inhibit the process of tumor necrosis factor alpha activate fat-storing cell,which was due to the apoptosis of fat-storing cells induced by interferon alpha1b.
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