实用药物与临床
實用藥物與臨床
실용약물여림상
PRACTICAL PHARMACY AND CLINICAL REMEDIES
2014年
5期
537-539,540
,共4页
氟尿嘧啶%肝癌%细胞凋亡%信号通路
氟尿嘧啶%肝癌%細胞凋亡%信號通路
불뇨밀정%간암%세포조망%신호통로
Fluorouracil%Hepatic carcinoma%Apoptosis%Signaling pathway
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。
目的:研究氟尿嘧啶(5-Fu)通過激活促凋亡信號通路介導人肝癌細胞(HepG-2)凋亡的治療作用。方法體外培養HepG-2細胞,分彆在0(空白對照組)、40、80、160μM濃度5-Fu榦預72 h,採用四甲基偶氮唑鹽(MTT)法測定5-Fu對HepG-2的抑製作用,DAPI染色檢查細胞形態學的改變,Western blot法測定內源性Fas蛋白以及cleaved-caspase-8錶達水平。結果與空白對照組比較,5-Fu榦預組明顯抑製HepG-2的細胞增殖(P<0.01),誘導細胞凋亡。此外,5-Fu可有效上調HepG-2內源性Fas蛋白和cleaved-caspase-8錶達水平(P<0.01)。結論氟尿嘧啶介導的抗肝癌作用是通過抑製HepG-2細胞增殖和激活內源性Fas信號通路而誘導癌細胞凋亡。
목적:연구불뇨밀정(5-Fu)통과격활촉조망신호통로개도인간암세포(HepG-2)조망적치료작용。방법체외배양HepG-2세포,분별재0(공백대조조)、40、80、160μM농도5-Fu간예72 h,채용사갑기우담서염(MTT)법측정5-Fu대HepG-2적억제작용,DAPI염색검사세포형태학적개변,Western blot법측정내원성Fas단백이급cleaved-caspase-8표체수평。결과여공백대조조비교,5-Fu간예조명현억제HepG-2적세포증식(P<0.01),유도세포조망。차외,5-Fu가유효상조HepG-2내원성Fas단백화cleaved-caspase-8표체수평(P<0.01)。결론불뇨밀정개도적항간암작용시통과억제HepG-2세포증식화격활내원성Fas신호통로이유도암세포조망。
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.