摘要
目的探讨姜黄素(Cur)对鱼藤酮(Ro)致PC12细胞损伤的保护作用及其机制。方法用鱼藤酮建立PC12细胞损伤模型;用四氮唑盐(MTT)比色法检测细胞增殖活力;苏木精-伊红染色观察细胞形态学变化;比色法检测细胞内总超氧化物歧化酶(SOD)的活性;DCFH-DA染色检测细胞内活性氧类物质(ROS)水平;流式细胞术(AnnexinⅤ-FITC/PI双染法)检测PC12细胞的凋亡。结果0.5μmol/L姜黄素和1.0μmol/L姜黄素均可减轻0.1μmol/L鱼藤酮对PC12细胞增殖活力的抑制,与鱼藤酮组比较差异有统计学意义(P<0.01);明显减轻了细胞损伤的形态学改变;明显增加了PC12细胞内SOD的活性,与鱼藤酮组比较差异有统计学意义(P<0.05);明显降低了PC12细胞内ROS的含量,明显抑制了鱼藤酮对PC12细胞凋亡的诱导作用,与鱼藤酮组比较差异均有统计学意义(均P<0.01)。结论姜黄素可拮抗鱼藤酮致PC12细胞的损伤,其机制可能与清除细胞内ROS,诱导抗氧化酶的活性有关。
Objective To investigate the cytoprotection of curcumin against rotenone（Ro）-induced injury and the molecular mechanisms underlying in PC12 cells. Methods The insulted model of PC12 cells was established with Ro. Cell viability was determined using MTT reduction assay. The content of reactive oxygen species（ROS）was determined by the method of DCFHDA staining. Chromatometry was used to measure the total activity of SOD,DCFH-DA staining to measure the level of intracellular ROS,and flow cytometry to assay the apoptosis rate. Results 0.5 and 1.0 μmol/L curcumin significantly decreased the inhibitory rate of Ro on the growth of PC12 cells for 24 h as compared with the Ro group（P〈0.01）. 0.5 and 1.0μmol/L curcumin significantly ameliorated the changes in morphology of PC12 cells,increased the activities of intracellular SOD as compared with the Ro group（P〈0.05） ,decreased the production of intracellular ROS and inhibited the apoptosis of PC12 cells induced by Ro for 24 h as compared with Ro group（P〈0.01）. Conclusion Curcumin can resist Ro-induced cytotoxicity probably by the mechanism of scavenging intracellular ROS and increasing the activity of antioxidase.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2010年第1期37-41,46,共6页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
