黄芪甲苷对胃癌细胞SGC7901侵袭能力的影响及其机制探讨

摘要

目的：研究黄芪甲苷对胃癌细胞SGC7901侵袭能力的影响并探讨其可能的机制。方法：用终浓度为100μg ／m l黄芪甲苷处理实验组细胞48 h ，之后采用流式细胞仪检测对照组和实验组细胞凋亡情况，T ransw ell细胞侵袭实验检测黄芪甲苷对细胞侵袭能力的影响，并采用PCR和Western‐blot方法检测黄芪甲苷对细胞MMP‐2和MMP‐9表达的影响，最后采用Western‐blot方法检测黄芪甲苷处理对细胞ERK通路的活化情况的影响。结果：100μg／ml黄芪甲苷处理胃癌细胞S G C790148 h后，细胞凋亡比例未发生明显变化，细胞侵袭能力显著降低，M M P‐2和M M P‐9分子的m RN A和蛋白水平均下降，此外，细胞内的磷酸化ERK蛋白水平在黄芪甲苷处理后表达减少。结论：在体外黄芪甲苷能够通过减少细胞MMP‐2和MMP‐9的表达而发挥抑制胃癌细胞侵袭的能力，而且其抑侵袭作用一定程度上是通过抑制细胞外信号调节激酶（ERK ）信号通路实现的。%Objective:To investigate the effects of astragaloside IV on the invasive capacity of gastric canc‐er cell line SGC7901 and to explore the potential mechanisms involved .Methods:The SGC7901 cell was treated with or without 100μg/ml astragaloside IV for 48h .After astragaloside IV administration ,the apoptotic cells between the control group and the experimental group were detected by flow cytometry ,the invasive capacity was measured by tr‐answell invasion assay ,the expression of MMP‐2 and MMP‐9 was leveled by PCR and Western‐blot .Finally ,the status of the ERK pathway was analyzed by Western‐blot to further elucidate the impact of astragaloside IV on SGC7901 cells .Results :After being treated with or without 100μg/ml astragaloside IV for 48h ,the SGC7901 cell possessed non‐significant proportion of apoptosis .The invasive capacity ,the MMP‐2 and the MMP‐9 expression were obviously impaired after astragaloside IV treatment .Besides ,Western‐blot assay showed that the phosphorylation of ERK was decreased in the experimental group .Conclusion:Astragaloside IV can inhibit the invasive capacity of gas‐tric cancer cells through diminishing the MMP‐2 and the MMP‐9 expression .And the anti‐invasion effects of astra‐galoside IV is possibly mediated by inactivating the ERK pathway .