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机构地区:[1]山东省立医院肝病科,山东济南250021 [2]山东省千佛山医院消化科,山东济南250014 [3]山东省医学科学院基础所,山东济南250062
出 处:《山东大学学报(医学版)》2007年第6期582-585,共4页Journal of Shandong University:Health Sciences
基 金:山东省自然科学基金资助课题(Y2002C45)
摘 要:目的:探讨肝癌细胞株HepG2.2.15通过低表达Fas逃避免疫监视,以及干扰素α(IFN-α)通过上调Fas表达对细胞凋亡的影响。方法:用流式细胞术检测肝癌细胞株HepG2.2.15的Fas表达及IFN-α对其Fas表达的影响;用激活性Fas单克隆抗体CH11诱导细胞凋亡的方法,研究肝癌细胞对Fas介导凋亡的抵抗以及IFN-α对肝癌细胞凋亡的影响。结果:①HepG2.2.15细胞低表达Fas,经浓度分别为2 000、1 000、500 U/ml的IFN-α作用后,Fas表达均显著增加(P均<0.001),且Fas表达率随IFN-α浓度的增加而增加;②CH11不能诱导HepG2.2.15细胞凋亡,IFN-α上调细胞Fas表达后,由CH11诱导的细胞凋亡增加(P均<0.01),且凋亡率随IFN-α浓度的增加而增加。结论:肝癌细胞HepG2.2.15能抵抗Fas介导的凋亡,IFN-α可通过上调细胞Fas表达,促进CH11诱导的肝癌细胞凋亡。Objective: To investigate the immune escape of hepatoma cell line HepG2.2.15 with low Fas expression as well as the effect of interferon-α(IFN-α) on the apoptosis in heptoma cells through up-regulating Fas expression. Methods: Flow cytometry was used to determine the Fas expression of the hepatoma cell line HepG2.2.15 and that treated with IFN-α. Resistance of hepatoma ceils to Fas- mediated apoptosis and the effect of IFN-α on the apoptosis were studied using anti-Fas agonistic monoclonal antibody CH11. Results: ①Fas expression of HepG2.2.15 was low and increased after the ceils were treated with IFN-α; ②CH11 could not induce HepG2.2.15 cells to apoptosis. But the apoptosis induced by CHll increased when the cells up-regulated the Fas expression after treatment with IFN-α. Conclusions: The hepatoma ceil line HepG2.2.15 could resist Fas-mediated apoptosis. IFN-α is able to up-regulate the Fas expression and subsequently promotes the CH11-mediated apoptosis.
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