丹参酮ⅡA对人胃癌细胞株MKN-45体外侵袭和转移能力的影响

目的：探讨丹参酮ⅡA对人胃癌细胞株MKN45体外侵袭转移能力的影响及其作用机制。方法：MKN45细胞体外培养,MTT法检测细胞增殖抑制率,细胞黏附侵袭实验检测细胞侵袭能力的改变,western blot检测各组培养细胞E-cadherin、CD44V6蛋白表达的变化。结果：与对照组比较,丹参酮ⅡA呈时间剂量性抑制胃癌MKN45细胞的增殖;各浓度丹参酮ⅡA处理组MKN45细胞与Matrigel胶的异质性黏附和侵袭、趋化能力均明显受抑制,有明显的剂量依赖性。western blot显示,丹参酮ⅡA能显著降低CD44V6蛋白、并上调E-cadherin蛋白的表达,与对照组相比,两者均剂量效应性显著。而不同时间组比较,E-cadherin蛋白按72h〈48h略呈负相关趋势（P〈0.05）,CD44V6蛋白的时间梯度差异性不很明显（P〉0.05）。结论：丹参酮ⅡA能抑制胃癌MKN45细胞侵袭和转移,其机制可能与直接抑制细胞侵袭转移活动,抑制MKN-45细胞相关基因蛋白CD44V6,促进黏附分子E-cadherin蛋白表达有关。

The infection of the ability of invasion and metastasis of tanshinone II A on human gastric cancer cell line MKN -45 in vitro

Objective：To discuss the infection of invasion and metastasis of tanshinone II A on human gastric cancer cell line MKN - 45 in vitro and its mechanism. Methods ： To culture MKN45 cells in vitro, detect cell proliferation inhibition rate in MTr , detect changes in cell invasion ability in cell adhesion invasion experiment, detect changes of E - cad- herin, CD44V6 protein expression of cultured cells each group in western blotin. Results ： Compared with the control group, tanshinone I1 A inhibited MKN45 gastric cancer cells proliferation by time - dose ; the groups of different concentrations of tanshinone II A treatmented , their MKN45 cells and the heterogeneity of plastic Matrigel were significantly inhibited in adhesion, invasion and chemotaxis ability , with a clear dose - dependent. Western blot showed that tanshinone II A can significantly reduce CD44V6 protein, and increase E -cadherin protein expression, compared with the control group, both showed dose effect significantly. The group at different times, E -cadherin protein is slightly negative correlation trend by 72h 〈 48h （ P 〈 0. 05 ）, the time grads diversity of CD44V6 protein is not obvious （ P 〉 O. 05 ）. Conclusion ： Tanshinone 11 A can inhibit invasion and metastasis of MKN45 gastric cancer cell , its mechanism may be related to direct inhibition of cell invasion and metastasis activity,inhibition of MKN -45 cellrelated gene protein CD,4V6, to promote the adhesion molecule E -cadherin protein expression.