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维生素K_3促肝癌细胞凋亡的实验研究 被引量:6

An experimental study on vitamin K3 induced HEPG2 cell line apoptosis
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摘要 目的观察维生素K3(VitK3)对肝癌细胞系HEPG2、Caspase3、BCL2基因的凋亡诱导作用。方法将不同浓度的VitK3作用于HEPG2细胞观察其作用的时间效应及剂量效应,应用细胞形态学,流式细胞术,DNA凝胶电泳等方法检测细胞凋亡的发生。应用逆转录聚合酶链反应(RTPCR)法检测凋亡相关基因Caspase3,Bcl2mRNA表达的变化。结果VitK3对HEPG2细胞的生长有明显的抑制作用,并诱导肿瘤细胞发生凋亡;细胞体积缩小,核固缩,折光性加强;DNA凝胶电泳显示DNALadder在G1期之前出现SubG1峰。凋亡相关基因Caspase3转录水平比用药前增强。结论VitK促HEPG2细胞凋亡,且与Caspase3基因表达有关。 Objective To study the effect of vitamin K3 (VitK3) on the apoptosis of human hepatocellular carcinoma cell line of HEPG2 and its relationship with Caspase-3 and Bcl-2 gene. Method With the treatment of VitK3, time and dosage effect was detected by MTT colorimetry. Appoptosis was observed by morphology, flow cytometry and DNA agarose gelelectrophoresis.Caspase-3 and Bcl-2 mRNA expression was assessed by RT-PCR. ResultVitK3 significantly inhibits HEPG2 cell proliferation and induce apoptosis.Caspase-3 mRNA expression was upregulated. ConclusionVitK3 induces HEPG2 cell apoptosis by way of Caspase-3 gene expression.
出处 《中华普通外科杂志》 CSCD 北大核心 2005年第6期365-367,共3页 Chinese Journal of General Surgery
关键词 维生素K3 肝癌细胞 细胞凋亡 肝细胞 维生素K CASPASE-3 BCL-2 Carcinoma, hepatocellular Vitamin K Apoptosis Caspase-3 Gene, Bcl-2
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同被引文献84

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