熊果酸诱导脑胶质瘤U251细胞株凋亡及其机制

目的：探讨熊果酸(Ursolic acid, UA)诱导脑胶质瘤U251细胞株凋亡的作用及机制。方法：培养脑胶质瘤细胞株(U251)，应用流式细胞仪观察UA对细胞周期的影响；琼脂糖凝胶电泳观察细胞DNA的变化；Western-blot测定COX-2及凋亡相关蛋白Bcl-2、Bax表达。放射免疫分析法测定COX-2催化产物前列腺素E2(prostaglandin E2, PGE2)。结果：流式细胞术及琼脂糖凝胶电泳均显示UA诱导U251细胞凋亡，细胞核DNA 呈梯状降解。同时COX-2蛋白表达及其催化生成产物PGE2浓度下降，凋亡相关蛋白Bcl-2表达减少，而Bax无明显变化。结论：熊果酸能明显诱导U251细胞凋亡，其机制可能与阻滞细胞周期、抑制COX-2表达、减少PGE2生成及下调凋亡抑制蛋白Bcl-2表达有关。

Effects of Ursolic acid on the apoptosis of glioma U251 cell line

Objective To investigate the role of ursolic acid(UA) in the apoptosis of glioma cell U251 in vitro and its mechanism.Methods Cell culture was performed.Then the effects of UA on the cell cycle were observed by flow cytometry,the change of DNA was observed by agarose gel electrophoresis,the expressions of COX-2,Bax,and Bcl-2 were detected by Western blot,and prostaglandin E2(PGE2) level was measured by radioimmunoassay.Results UA significantly induced the apoptosis of the cell.PGE2 level and both COX-2 and Bcl-2 expressions were declined,while Bax expression did not differ significantly.Conclusion UA can markedly induce the apoptosis of the cell U251,whose mechanism is associated with arresting cell cycle,inhibiting COX-2 expression to reduce PGE2 production,and downregulating Bcl-2 expression.