三氧化二砷诱导大鼠血管平滑肌细胞凋亡的实验研究

Experimental study of vascular smooth muscle cell apoptosis induced by arsenic trioxide in rats

目的 探讨三氧化二砷抗动脉粥样硬化的效应及机制。方法 建立大鼠主动脉血管平滑肌增殖模型。通过四氮唑蓝还原反应、免疫组化、Western印迹观察三氧化二砷作用后细胞凋亡和诱导机制。结果 免疫组化、Western印迹显示随三氧化二砷浓度的增高及作用时间的延长 ,Bcl 2蛋白表达下降。结论 三氧化二砷诱导VSMCs凋亡的机制可能是通过下调过度表达的Bcl

OBJECTIVE: To investigate the antiatherogenetic effect of arsenic trioxide and its mechanisms. METHODS: VSMCs proliferation model of cultured rat thoracic aorta was established. NBT reduction test, immunohistochemical staining, western blot were applied respectively to observe the apoptotic changes. RESULTS: The results of immunohistochemical staining and western blot showed the expression of Bcl-2 decreased in concentration- and time-dependency. CONCLUSION: Arsenic trioxide can induce apoptosis of rat proliferated VSMCs, and this mechanism maybe the expression of Bcl-2 protein downregulated.