目的 研究冬凌草甲素（ORI）對人結(jié)腸癌細(xì)胞SW620的增殖抑制、誘導(dǎo)凋亡作用，并探討其可能的分子機制。方法 采用結(jié)晶紫染色研究ORI（5、10、15、20、25 μmol/L）對SW620細(xì)胞的增殖抑制作用；流式細(xì)胞術(shù)研究ORI（10、15、20 μmol/L）誘導(dǎo)SW620細(xì)胞凋亡作用；采用Western blotting技術(shù)研究ORI對SW620細(xì)胞中增殖細(xì)胞核抗原（PCNA）、凋亡相關(guān)指標(biāo)（Caspase-3）、骨形態(tài)發(fā)生蛋白7（BMP7）、p53蛋白表達的影響；轉(zhuǎn)染重組p53腺病毒實現(xiàn)p53的外源性過表達，p53抑制劑PFTα降低BMP7水平，檢測ORI是否通過調(diào)節(jié)p53表達影響細(xì)胞增殖凋亡、BMP7-p53信號通路。結(jié)果 與對照組比較，ORI可以時間和劑量依賴性地抑制SW620細(xì)胞生長，上調(diào)PCNA蛋白水平；流式細(xì)胞術(shù)以及Western blotting檢測結(jié)果顯示，ORI明顯增加細(xì)胞凋亡率，促進Caspase-3蛋白表達，并且上調(diào)BMP7和p53蛋白表達；外源性過表達p53加強了ORI對上述蛋白表達的調(diào)控，PFTα則部分抑制了ORI的作用。結(jié)論 ORI可以通過激活BMP7-p53信號通路抑制SW620細(xì)胞增殖、誘導(dǎo)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.

重慶市渝中區(qū)科委課題（20150120）