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目的探讨双氢青蒿素对胶质瘤细胞C6生长影响及可能机制。方法培养大鼠脑胶质瘤C6细胞,噻唑蓝法检测双氢青蒿素对C6细胞生长抑制率,annexin V/PI检测C6细胞凋亡率;ELISA法检测细胞培养液上清中cyclin D1、Bax和casepase-3蛋白表达变化;Western blot法检测Bax和Bcl-2蛋白表达量。结果双氢青蒿素可明显抑制C6细胞生长,以作用48 h最为明显,0.05、0.50、5.00和50.00μmol/L双氢青蒿素组细胞生长抑制率分别为(83.96±1.08)%、(74.04±3.54)%、(68.70±9.20)%和(57.25±7.01)%,与对照组(100.00±1.07)%比较,差异有统计学意义(P<0.01);50.00μmol/L双氢青蒿素组细胞凋亡率[(25.98±3.95)%]明显高于对照组[(2.32±0.78)%],差异有统计学意义(P<0.01);与对照组比较,各剂量双氢青蒿素组C6细胞培养液上清中caspase-3分泌增加,50.00μmol/L双氢青蒿素组细胞Bax蛋白表达增加,Bcl-2蛋白表达减少,Bax/Bcl-2比值增加。结论双氢青蒿素通过下调cyclin D1蛋白,上调Bax/Bcl-2比值使caspase-3蛋白活化,从而抑制胶质瘤细胞生长。
Objective To investigate the effects of dihydroartemisinin on C6 glioma cells and its possible mechanism. Methods The C6 glioma cells were cultured in vitro. The inhibitory rate of dihydroartemisinin to C6 cells was detected by the thiazolyl blue method and the apoptosis rate of C6 cells was analyzed by annexin V / PI. The expressions of cyclin D1, Bax and casepase-3 protein expression; Western blot detection of Bax and Bcl-2 protein expression. RESULTS: Dihydroartemisinin significantly inhibited the growth of C6 cells and the most obvious effect was at 48 h. The inhibition rates of dihydroartemisinin group were (83.96 ± 1.08)%, (0.05 ± 0.50), 5.00 and 50.00 μmol / L 74.04 ± 3.54%, 68.70 ± 9.20% and 57.25 ± 7.01%, respectively, which was significantly different from that of the control group (100.00 ± 1.07)% (P <0.01) (25.98 ± 3.95)%] was significantly higher than that of the control group [(2.32 ± 0.78)%], the difference was statistically significant (P <0.01). Compared with the control group, The secretion of caspase-3 in the supernatant of C6 cell culture supernatant increased, the expression of Bax protein increased, the expression of Bcl-2 protein decreased and the ratio of Bax / Bcl-2 increased in 50.00μmol / L dihydroartemisinin group. Conclusion Dihydroartemisinin can inhibit the growth of glioma cells by down-regulating cyclin D1 protein and increasing the ratio of Bax / Bcl-2 to caspase-3 protein.