氟尿嘧啶通过激活促凋亡信号通路介导人肝癌细胞凋亡的治疗作用

氟尿嘧啶通过激活促凋亡信号通路介导人肝癌细胞凋亡的治疗
作用
任召磊
【期刊名称】《实用药物与临床》
【年(卷),期】2014(17)5
【摘要】目的：研究氟尿嘧啶(5-Fu)通过激活促凋亡信号通路介导人肝癌细胞(HepG-2)凋亡的治疗作用。

方法体外培养HepG-2细胞,分别在0(空白对照组)、40、80、160μM浓度5-Fu干预72 h,采用四甲基偶氮唑盐(MTT)法测定5-Fu对HepG-2的抑制作用,DAPI染色检查细胞形态学的改变,Western blot法测定内源性Fas蛋白以及cleaved-caspase-8表达水平。

结果与空白对照组比较,5-Fu干预组明显抑制HepG-2的细胞增殖(P<0．01),诱导细胞凋亡。

此外,5-Fu可有效上调HepG-2内源性Fas蛋白和cleaved-caspase-8表达水平(P<0．01)。

结论氟尿嘧啶介导的抗肝癌作用是通过抑制HepG-2细胞增殖和激活内源性Fas信号通路而诱导癌细胞凋亡。

%Objective To investigate the therapeutic effect of fluorouracil mediating apoptosis-related in hu-man hepatoma carcinoma cells through activating the pro-apoptotic signaling pathway. Methods Cultured HepG-2 cells in vitro,the medication was treated with 0 (blank control group),40,80,160 μM 5-Fu concentration for 72 h,re-spectively. The inhibition effect of 5-Fu on HepG-2 was employed using the methylthiazolyl tetrazolium ( MTT) assay;morphological changes of HepG-2 was assessed through DAPI staining;endogenous expression of Fas and cleaved-caspase-8 in HepG-2 was measured by Western blotting assay.
Results Compared with the blank control group,5-Fu treated groups significantly inhibited the proliferation of HepG-2 cells (P<0. 01),and induced apoptosis. Additionally, 5-Fu treatment effectively up-regulated the endogenous Fas and cleaved-caspase-8 levels in HepG-2 ( P<0. 01 ) . Con-clusion Fluorouracil-mediated antihepatocarcinoma role was via inhibiting HepG-2 cell proliferation and activating en-dogenous Fas signaling pathway to induce apoptosis in liver cancer.
【总页数】4页(P537-539,540)
【作者】任召磊
【作者单位】山东省淄博矿业集团有限责任公司中心医院，山东淄博255100【正文语种】中文
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