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目的:探讨葫芦素I对肝癌细胞生长的抑制作用及机制.方法:采用CCK-8法检测葫芦素I对不同肝癌细胞(HepG2、QGY-7703、SMMC-7721)增殖活力的影响;葫芦素I处理HepG2细胞后,分别用细胞平板克隆形成实验、流式细胞术、Hochest 33342染色观察细胞克隆形成、细胞周期、凋亡情况,并用Western blot和qRT-PCR检测抗凋亡因子及其相关信号分子蛋白和mRNA表达变化.结果:葫芦素I处理后,不同肝癌细胞的增殖均明显抑制,并呈时间与浓度依赖性(均P<0.05);葫芦素I对HepG2、QGY-7703、SMMC-7721细胞48 h的IC50值分别为0.19、4.16、1.13μmol/L.HepG2细胞经葫芦素I处理24 h后,克隆形成几乎被完全抑制,出现典型的细胞凋亡形态变化和明显的G2期阻滞;抗凋亡因子Mcl-1、survivin以及转录因子STAT3蛋白与mRNA的表达均明显下调,mRNA半定量分析显示差异均有统计学意义(均P<0.05).结论:葫芦素I抑制肝癌细胞的生长,其作用机制可能与STAT3通路下调抗凋亡相关蛋白表达,从而增加细胞凋亡有关.“,”Objective: To investigate the influence of cucurbitacin I on growth of hepatocellular carcinoma (HCC) cells and the mechanism.Methods: The influences of cucurbitacin I on proliferative activities of different types of HCC cells (HepG2, QGY-7703 and SMMC-7721) were measured by CCK-8 assay. In HepG2 cells after treatment with cucurbitacin I, the colony formation, cell cycle profile and apoptosis were examined by plate colony-forming assay, flow cytometry and Hochest 33342 staining, and the protein and mRNA expressions of anti-apoptotic factors and their related signaling molecules were determined by Western blot analysis and qRT-PCR method, respectively. Results: The proliferations of all the selected HCC cells were significantly inhibited by cucurbitacin I treatment, with a time- and concentration-dependent manner (all P<0.05), and the 48-h IC50 value of cucurbitacin I for HepG2, QGY-7703 and SMMC-7721 was 0.19, 4.16 and 1.13 μmol/L, respectively. In HepG2 cells after cucurbitacin I treatment for 24 h, the clone formation was almost completely suppressed, typical apoptotic morphological changes and evident G2-phase arrest were presented, and both protein and mRNA expressions of the anti-apoptotic factors Mcl-1 and survivin as well as the transcription factor STAT3 were markedly down-regulated, and the semi-quantitative analysis of mRNA expressions showed all differences had statistical significance (all P<0.05). Conclusion: Cucurbitacin I can suppress the growth of HCC cells, and the mechanism may be associated with its down-regulating the expressions of anti-apoptotic factors through STAT3 signaling pathway, and thereby inducing cell apoptosis.