三氧化二砷诱导大鼠血管平滑肌细胞凋亡的实验研究

目的探讨三氧化二砷(As2O3)诱导血管平滑肌细胞(VSMCs)凋亡的机制。方法建立大鼠胸主动脉血管平滑肌细胞增殖模型。通过透射电镜、流式细胞仪观察As2O3作用后细胞凋亡形态学和细胞胞浆游离钙离子(Ca^2 )浓度的变化。结果经As2O3处理的VSMCs电镜下呈现凋亡的特征性改变，形态学上表现为细胞胞膜完整、染色质固缩及核碎裂。流式细胞仪分析显示，VSMCs在As2O3作用后出现凋亡峰，而As2O3能通过促进细胞外Ca^2 内流和细胞内Ca^2 池的释放提高胞浆游离Ca^2 浓度。结论As2O3可诱导VSMCs凋亡，并可能与胞浆游离Ca^2 浓度升高有关。

Experimental study on vascular smooth muscle cell apoptosis induced by arsenic trioxide

Objective To appraise the apoptosis mechanism of vascular smooth muscle cells (VSMCs) by Arsenic trioxide.Methods VSMCs proliferation model of cultured rat thoracic aorta was constructed. Flow cytometry (FCM) and Transmission eletronmicroscopy (TEM) were used to observe the characteristic apoptosis changes in morphology and intracellular calcium concentration for study and interpretation of the mechanism.Results VSMCs treated by Arsenic trioxide presented some morphological features of apoptotic cell under TEM such as intact cell membrane, chromatin condensation and nuclear fragmentation. Apoptotic peak was observed by FCM after treatment presenting increased of the free intracytoplasmic calcium concentration not only by inflow of extracellular Ca 2+ but also by the Ca 2+ released from intracellular calcium store. Conclusion Arsenic trioxide can induce apoptosis of rat proliferated VSMC, which is related to the increase of intracytoplasmic free Ca 2+ concentration.