目的 研究冬凌草甲素（ORI）对人结肠癌细胞SW620的增殖抑制、诱导凋亡作用，并探讨其可能的分子机制。方法 采用结晶紫染色研究ORI（5、10、15、20、25 μmol/L）对SW620细胞的增殖抑制作用；流式细胞术研究ORI（10、15、20 μmol/L）诱导SW620细胞凋亡作用；采用Western blotting技术研究ORI对SW620细胞中增殖细胞核抗原（PCNA）、凋亡相关指标（Caspase-3）、骨形态发生蛋白7（BMP7）、p53蛋白表达的影响；转染重组p53腺病毒实现p53的外源性过表达，p53抑制剂PFTα降低BMP7水平，检测ORI是否通过调节p53表达影响细胞增殖凋亡、BMP7-p53信号通路。结果 与对照组比较，ORI可以时间和剂量依赖性地抑制SW620细胞生长，上调PCNA蛋白水平；流式细胞术以及Western blotting检测结果显示，ORI明显增加细胞凋亡率，促进Caspase-3蛋白表达，并且上调BMP7和p53蛋白表达；外源性过表达p53加强了ORI对上述蛋白表达的调控，PFTα则部分抑制了ORI的作用。结论 ORI可以通过激活BMP7-p53信号通路抑制SW620细胞增殖、诱导凋亡。

Objective To investigate the proliferation inhibitory and apoptosis-inducing effects of oridonin (ORI) on human colon cancer SW620 cells and its possible mechanisms. Methods Crystal violet staining and flow cytometry assay were introduced to analyze the proliferation inhibition and induction apoptosis of ORI on SW620 cells. Western blotting assay were used to detect the effects of ORI on the expression of PCNA, Caspase-3, BMP7, and p53 of SW620 cells; The exogenous overexpression of p53 was achieved by transfecting recombinant adenovirus, and its inhibitor (PFTα) reduced the level of BMP7 with aim to detect the influence of ORI on the BMP7-p53 pathway. Results ORI (5, 10, 15, 20, and 25 μmol/L) could inhibit the proliferation of SW620 cells in a time and concentration dependent manner and upregulate the protein level of PCNA; Flow cytometry and Western blotting results showed that ORI induced apoptosis of SW620 cells significantly and upregulated the expression of BMP7, Caspase-3, and p53. The exogenous overexpression of p53 strengthened the expression regulation of above proteins, While p53 inhibitor (PFTα) reduced growth inhibition rate and apoptosis rate induced by ORI in SW620 cells and downregulated the level of BMP7 and p53. Conclusion ORI can induce apoptosis of SW620 cells via BMP7-p53 signal pathway.

重庆市渝中区科委课题（20150120）