目的 探究替莫唑胺对胶质瘤细胞U251凋亡的影响及其作用机制。方法 40、80、120 μmol/L替莫唑胺培养U251细胞系48 h，观察形态变化，流式细胞术检测细胞凋亡率，实时荧光定量PCR（qRT-PCR）法检测caspase 3表达，用caspase 3试剂盒检测caspase 3的活性，蛋白免疫印迹（Western blotting）法检测热休克蛋白90（HSP90）、p-HSP90、丝氨酸苏氨酸蛋白激酶（AKT）和p-AKT表达。结果 替莫唑胺80、120μmol/L组细胞数目减少，细胞核体积明显缩小，染色质固缩。替莫唑胺80、120 μmol/L组细胞凋亡率、caspase 3的表达水平和活性明显高于对照组，p-HSP90、p-AKT的表达水平明显低于对照组（P<0.05），呈剂量相关性。结论 替莫唑胺能够促进胶质瘤细胞U251凋亡，可能是通过抑制HSP90和AKT表达来实现的。

Objective To explore the influence of temozolomide on apoptosis of glioma cell line U251 and study its mechanisms. Methods U251 cell line were treated with 40, 80, and 120 μmol/L temozolomide for 48 h. Morphological changes were observed, and apoptosis rate was detected by flow cytometry. Caspase 3 expression was detected by using real-time quantitative PCR (qRT-PCR) method, and the activity of caspase 3 was tested by using caspase 3 Kit. HSP90, p-HSP90, AKT and p-AKT expressions were detected by Western blotting method. Results The number of cells decreased in 80 and 120 μmol/L temozolomide groups, and nucleus size decreased significantly, and chromatin contracted. The apoptosis rate and expression levels and activities of caspase 3 in 80 and 120 μmol/L temozolomide groups were significantly higher than those in the control group, but P-HSP90 and p-AKT expression levels were significantly lower than those in the control group (P < 0.05), and were in a dose manner. Conclusion Temozolomide can promote the apoptosis of glioma cell line U251, and it may be achieved by inhibiting the expression of HSP90 and AKT.