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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。
Objective: To investigate the effects of chikusetsu saponin iva methyl (CSIM) on proliferation of vascular smooth muscle cells (VSMCs) stimulated by angiotensin II (Ang-II) and its mechanism. Methods: Rat vascular smooth muscle cells were used as experimental subjects to establish a proliferation model of VSMCs stimulated by Ang-II. The cytotoxicity of CSIM to VSMCs was detected by MTT assay. The effects of CSIM on the proliferation of VSMCs were detected by CCK-8 assay and BrdU assay. The migration of VSMCs was detected by scratch assay. The protein expression of PTEN and NF-κB was detected by Western blotting. . Results: CSIM at 3μmol / L significantly inhibited the proliferation (P <0.05) and the migration of VSMCs induced by Ang-II (P <0.05), accompanied by the marked upregulation of PTEN protein and the expression of NF- κB protein Significantly decreased (P <0.05). CONCLUSION: CSIM can inhibit the proliferation and migration of VSMCs induced by Ang-II. The mechanism may be related to the upregulation of PTEN protein and the decrease of NF-κB protein expression.