中文摘要：

目的研究蜂毒素对人肝癌HepG2细胞增殖和凋亡的影响,并探讨其作用和HDAC2及Hedgehog信号通路的关系。方法给予不同浓度蜂毒素,四甲基偶氮唑盐（MTT）法检测HepG2细胞的增殖变化,Hoechst33258染色和流式细胞术检测HepG2细胞凋亡变化;qRT-PCR检测SHH、PTCH1、SMO、Gli1、HDAC2 mRNA的表达;Western blot检测SHH、PTCH1、SMO、Gli1、HDAC2蛋白的表达。结果不同浓度的蜂毒素在作用48 h后,能明显抑制Hep G2细胞的增殖,促进其凋亡;Hedgehog信号通路中SHH、PTCH1、SMO、Gli1 mRNA及蛋白水平均明显降低,并与蜂毒素浓度呈负相关。同时检测到细胞内HDAC2 mRNA及蛋白水平均降低,与蜂毒素剂量呈负相关。结论蜂毒素可明显抑制人肝癌Hep G2细胞增殖,促进其凋亡,其作用与抑制HDAC2,下调Hedgehog信号通路密切相关。

英文摘要：

Aim To observe the effect of melittin on human hepatocelluar carcinoma HepG2 cell proliferation in vitro and its further mechanisms. Methods The capacity of cellular proliferation and apoptosis was measured with the 3-（ 4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide（ MTT） assay,Hoechst33258 assay and Annexin V-FITC / PI assay. The mRNA expression of Shh, PTCH1, SMO, GLi1 and HDAC2 was performed by qRT-PCR. And the protein expression of Shh,PTCH1,SMO,GLi1 and HDAC2 was assessed by western blotting. Results Our study found that melittin effectively inhibited cell proliferation and promoted cell apoptosis in vitro using MTT method and Flow cytometry. The mRNA and protein expression of Shh,PTCH1,SMO,GLi1 and HDAC2 were obviously decreased after treated with various concentrations of melittin for 48 h in Hep G2 cells. Conclusions Taken together,our data suggest that melittin could inhibit cell proliferation and promote cell apoptosis,reduce the level of HDAC2 and down-regulate the Hedgehog signaling pathway in this process simultaneously.