粉防己碱对血管内皮剥脱后再狭窄的预防作用及其分子机制研究

PROTECTION OF TETRANDRINE ON RESTENOSIS AFTER VASCULAR ENDEPIDERMIS AND ITS MOLECULE MECHANISM

目的研究球囊损伤后血管平滑肌细胞 (vascularsmoothmusclecells,VSMC)凋亡机制及粉防已碱(tetrandrine ,Tet)对VSMC凋亡及凋亡相关基因表达的影响。方法采用末端脱氧核苷酸转移酶介导的三磷酸脱氧尿嘧啶缺口末端标记法和免疫组化技术检测球囊损伤内皮后VSMC凋亡及bcl 1、bax蛋白表达的变化。结果球囊损伤后血管壁增生 ,血管中膜和内膜出现的细胞凋亡较少。Tet可明显促进VSMC凋亡、降低球囊损伤后内膜及中膜厚度、增加管腔面积 (P <0 .0 5 ) ,促进bax蛋白的表达、抑制bcl 2蛋白的表达 (P <0 .0 5 )。结论bax、bcl 2参与了球囊损伤内皮后血管平滑肌细胞凋亡的调节 ,Tet可能通过对bax、bcl 2基因表达的调节 ,增加VSMC细胞凋亡 。

ObjectiveTo investigate the mechanism of vascular smooth muscle cells(VSMC) apoptosis after balloon injury. To study the effect of tetrandrine(Tet) on the apoptosis and apoptosis related gene expression of VSMC.MethodsApoptosis of VSMC, and expression of bax and bcl 2 at protein level were studied by TUNEL and immunohistochemical technique after balloon injury.ResultsAfter balloon injury, the blood vessel proliferated. Apoptosis of VSMC appeared in intima and media of the blood vessel. Tet significantly increased the apoptosis of VSMC,but decreased the thickness of intima and media after balloon injury (P< 0.05 ), and also increased the area of vascular lumina. Tet significantly increased the expression of bax protein and decreased the expression bcl 2 protein(P< 0.05 ).ConclusionBax and bcl 2 contribute to the regulation of VSMC apoptosis after balloon injury. Tet can increase the apoptosis of VSMC by the regulation of bax and bcl 2 gene.Tet could significantly inhibit VSMC proliferation and prevent the restenosis of blood vesses after balloon injury.