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为研究细胞因子对肾癌细胞株 786 0Fas表达以及FasAb介导凋亡的影响 ,单独或联合应用IFN γ ,IFN α ,IL 2 ,TNF α刺激 786 0细胞株 ,并以Fas单克隆抗体 (FasAb )诱导其凋亡。结果发现 ,IFN α、IFN γ均能显著上调 786 0细胞的Fas表达 (P <0 0 1,P <0 0 1)并促进FasAb诱导的凋亡 (P <0 0 1,P <0 0 1) ;IL 2、TNF α对 786 0的Fas表达及FasAb诱导的凋亡均无影响 ;IL 2不能增强IFN α、IFN γ诱导的Fas表达 ,亦不能促进凋亡。TNF α能增强IFN α诱导的Fas表达并促进凋亡 ,但不影响IFN γ诱导的Fas表达及其凋亡。结果表明IFN γ、IFN α可增强肾癌细胞株 786 0的Fas表达 ,并促进FasAb介导的凋亡。但其对FasAb介导凋亡的敏感性并不完全取决于Fas表达水平
In order to study the effect of cytokines on the expression of 786Fas and the FasAb-mediated apoptosis in human renal cell carcinoma cell line 786o, IFNα, IFNα, IL-2 and TNFα were treated alone or in combination with FasAb ) Induce its apoptosis. The results showed that both IFNα and IFNγ significantly up-regulated Fas expression in 786 0 cells (P <0.01, P <0.01) and promoted FasAb-induced apoptosis (P <0.01, P <0.01 ); IL 2, TNFα had no effect on the Fas expression of 786 0 and FasAb-induced apoptosis; IL 2 could not enhance the expression of Fas induced by IFNα, IFNγ, nor could it promote apoptosis. TNFα can enhance IFNα-induced Fas expression and promote apoptosis, but does not affect IFNγ-induced Fas expression and apoptosis. The results showed that IFNγ and IFNα can enhance the Fas expression in 786 0 cell line and promote FasAb-mediated apoptosis. However, its sensitivity to FasAb-mediated apoptosis does not depend entirely on the level of Fas expression