摘要
目的:探讨依达拉奉对硝普钠诱导的PC12细胞凋亡的影响。方法:体外培养PC12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检测凋亡抑制蛋白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PC12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PC12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。
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.
出处
《现代生物医学进展》
CAS
2013年第35期6900-6903,共4页
Progress in Modern Biomedicine