目的:探讨竹节参皂苷IVa甲酯(chikusetsu saponin iva methyl,CSIM)对血管紧张素II(angiotensin,Ang-II)刺激的血管平滑肌细胞(vascular smooth muscle cells,VSMCs)增殖的影响及机制研究。方法:以大鼠血管平滑肌细胞为实验对象,建立Ang-II刺激的VSMCs增殖模型。MTT法检测CSIM对VSMCs的毒性;CCK-8法、Brd U法检测CSIM对VSMCs增殖的影响,划痕实验检测CSIM对VSMCs迁移力的影响,免疫蛋白印迹法检测PTEN、NF-κB蛋白表达水平。结果:3μmol/L的CSIM可显著抑制Ang-II诱导的VSMCs增殖(P〈0.05)与迁移(P〈0.05),并伴随着PTEN蛋白的明显上调(P〈0.05)及NF-κB蛋白表达的显著性降低(P〈0.05)。结论:CSIM抑制Ang-II诱导的VSMCs增殖与迁移,其机制可能与上调PTEN蛋白,降低NF-κB蛋白表达有关。
AIM: To observe the effects and mechanism of chikusetsu saponin iva methyl to vascular smooth muscle cells( VSMCs) proliferation.METHODS: VSMCs was cultured in vitro and the cell proliferation model was established by Ang-II.The VSMCs toxicity were determined by MTT assay,the proliferation of VSMCs was detected by CCK-8and Brd U assay,the VSMCs migration distance was detected by wound-healing assay,the PTEN,NF-κB protein expression was determined by Western blot assay. RESULTS: 3 μmol / L of chikusetsu saponin iva methyl significantly inhibited the proliferation and migration of Ang-II-induced VSMCs( P〈0. 05),increased PTEN protein expression( P〈0. 05),reduced NF-κB protein expression( P〈0. 05). CONCLUSION: Chikusetsu saponin iva methyl can inhibit the proliferation and migration of Ang-II induced VSMCs,which may be related to regulating PTEN protein,reducing NF-κB protein expression.