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目的探讨西门木炔酸的抗结肠癌活性和相关机制。方法以}HCT116细胞为对象,用不同浓度和不同时间的西门木炔酸干预后,使用MTT法测细胞增殖活性、流式细胞仪测细胞凋亡和细胞周期情况,以及qPCR检测细胞周期相关因子的表达情况。结果西门木炔酸干预48h,显著抑制了HCT116的增殖活性(抑制浓度大于25μmol/L);干预72h,西门木炔酸25μmol/L时对HCT116细胞增殖的抑制率超过了50%。西门木炔酸也显著促进了HCT116晚期凋亡和坏死细胞的生成(25~100μmol/L)。西门木炔酸还显著阻滞HCT116细胞周期G1-S期的转变,表现为S期细胞显著下降(25~100μmol/L),并呈现时间和剂量依赖优势。此外,西门木炔酸干预下,HCT116细胞周期因子CCND3、CCNE1和CDK6的表达也显著下降(100μmol/L)。结论西门木炔酸显著抑制HCT116细胞增殖、促进细胞晚期凋亡和坏死,这与西门木炔酸抑制细胞周期因子表达进而阻滞HCT116细胞周期G1-S期的转变有关
Objective To investigate the anti-colon cancer activity and related mechanisms of ximenamycin. Methods HCT116 cells were treated with different concentrations and different times of ximenomu acid, MTT assay was used to measure cell proliferation, flow cytometry was used to measure apoptosis and cell cycle, and qPCR was used to detect cell cycle related factors The expression of the situation. Results The inhibitory rate of HCT116 proliferation was significantly inhibited by ximenuynynoic acid (48 h) for 48 h, and the inhibitory rate of HCMT116 cell proliferation exceeded 50% by 72 h with ximenomu acid 25 μmol / L. Simmonic acid also significantly promoted the generation of advanced apoptotic and necrotic cells of HCT116 (25-100 μmol / L). Simvastatin also significantly blocked the G1-S phase transition of HCT116 cells, showing a significant decrease (25-100 μmol / L) of S phase cells in a time- and dose-dependent manner. In addition, the expression of CCND3, CCNE1 and CDK6 in HCT116 cells was also significantly decreased (100μmol / L) with the addition of ximenamenic acid. Conclusion Ximenamycin significantly inhibits the proliferation of HCT116 cells and promotes the apoptosis and necrosis of cells in vitro, which is related to the inhibition of cell cycle factor expression and the block of G1-S phase transition in HCT116 cells