依达拉奉对硝普钠诱导的PC12细胞凋亡的保护作用

目的：探讨依达拉奉对硝普钠诱导的PCI2细胞凋亡的影响。方法：体外培养PCI2细胞，并分为依达拉奉对硝普钠保护组（含500μmol／L硝普钠和75μmol／L依达拉奉）、硝普钠诱导组（含500μmol／L硝普钠）和对照组。采用MTT法检测细胞的增殖率：流式细胞术检测细胞的凋亡情况；Western-blot检i受4凋亡抑制蛋白Bcl-2和凋亡促进蛋白Bad的表达。结果：与对照组相比，硝普钠处理的PCI2细胞增殖率显著降低，而细胞凋亡率显著升高，细胞内Bcl-2的表达显著减少，而Bad的表显著增加，差异均具有统计学意义（P〈0．05）；与单纯硝普钠诱导组相比，依达拉奉处理组细的胞增殖率显著增加而细胞凋亡率显著减少，同时Bcl－2的表达显著增加，而Bad的表达明显减少，差异均具有统计学意义（P〈0．05）。结论：依达拉奉对硝普钠诱导的PCI2细胞凋亡具有抑制作用，可能通过增加Bcl-2的表达并降低Bad的表达发挥抗凋亡作用。

The Effects of Edaravone on the Apoptosis in PC 12 Cells Induced by Sodium Nitroprusside

Objective：To investigate the effect of edaravone on the apoptosis in PC12 cells induced by sodium nitroprusside. Methods： PC12 cells were cultured in vitro and divided into three groups： the control group, sodium nitropmsside （SNP） group and edaravone （EDA） group. The proliferation of PC12 was measured by thiazolyl blue （MTT） assay. The cell apoptosis was determined by Annexin V-FITC flow cytometry. Western blotting was performed to detect the protein expression of Bad and Bcl-2. Results： Compared with the control group, the proliferation decreased and the apoptosis increased in PC 12 cells induced by sodium nitroprusside, the protein expression of Bcl-2 decreased and the protein expression of Bad increased significantly （P〈0.05）. Compared with SNP, EDA promoted the proliferation and inhibited the apoptosis in PC12. The expression of Bcl-2 increased and Bad decreased significantly after being treated with EDA in PCI2 （P〈0.05）. Conclusion： Edaravone could inhibit the apoptosis in PC12 cells induced by sodium nitroprusside, the decreased expression of Bad and increased expression of Bcl-2 may be involved in the anti-apoptosis of Edaravone.