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熊果酸诱导肝癌细胞HepG2凋亡的实验研究 被引量:2

Experimental Study on Ursolic Acid Inducing Apoptosis in Human Hepatocellular Carcinoma Cell Line HepG2
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摘要 目的:探讨熊果酸对肝癌细胞HepG2的增殖抑制和诱导凋亡作用及其机制。方法:运用体外细胞毒性实验(MTT)检测细胞的增殖;流式细胞术分析细胞周期和凋亡率;Western blot检测HepG2细胞内细胞色素C(cytochrome c,cyt-c)、caspase-3的表达。结果:熊果酸对HepG2细胞具有抑制增殖和诱导凋亡作用,并呈浓度和时间依赖性;细胞主要阻滞在G_0/G_1期,S期细胞数减少;同时cyt-c释放和caspase-3酶原活化增加。结论:熊果酸能够在体外抑制肝癌细胞HepG2增殖并诱导其凋亡,而促进cyt-c释放增加,引起caspase-3的活化可能是其作用机制之一。 Objective:To investigate whether ursolic acid can inhibit proliferation of human Hepatocellular carcinoma cell line HepG2 and induce apoptosis and its mechanism.Methods:Cell proliferation was determined by MTT assay.Cell cycle and apoptosis rate were analyzed by flow cytometry.The expression of cyt-c and caspase-3 were detected by western blotting.Results:MTT assay showed that UA had a moderate anti-proliferation effect on HepG2 cells in time-and-dose-dependant manner.Apparent morphological index of apoptosis was observed,cells mainly arrest in G_0/G_1 phase and S phase decline.The release of cyt-C and activation of caspase-3 were enhanced in vitro.Conclusion:UA can inhibit proliferation and induce apoptosis in HepG2.The mechanism may have to do with the induction of delivery of cyt-C and the activation of caspase-3.
作者 张静
机构地区 长江大学医学院
出处 《长江大学学报(自科版)(下旬)》 CAS 2010年第4期4-6,共3页 Journal of Yangtze University
关键词 熊果酸 HEPG2 细胞色素C CASPASE-3 Ursolic acid HepG2 Cytochrome C Caspase-3
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