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机构地区:[1]黑龙江中医药大学佳木斯学院,黑龙江佳木斯154007 [2]黑龙江中医药大学中医药研究院,黑龙江哈尔滨150040
出 处:《辽宁中医杂志》2010年第11期2243-2245,共3页Liaoning Journal of Traditional Chinese Medicine
基 金:国家"重大新药创制"科技重大专项"十一五"计划资助项目(2009ZX09103);黑龙江省教育厅海外学人科研资助项目(1153h18)
摘 要:目的:考察MPP+诱导PC12细胞氧化应激损伤作用,并探讨其机制。方法:以不同浓度、不同作用时间的MPP+作用于PC12细胞,MTT法检测细胞存活率,流式细胞仪测细胞凋亡率,紫外可见分光光度计测LDH、NO、NOS、MDA含量和SOD活性。结果:MPP+终浓度达到300μmol/L时,作用48h后可明显降低PC12细胞存活率(P<0.001),提高细胞凋亡率(P<0.01),增强LDH、NO、NOS、MDA的含量和降低SOD活性,有统计学意义(P<0.05)。结论:MPP+能诱导PC12细胞氧化应激损伤,其作用机制可能是通过增加PC12细胞NO和NOS含量,引起胞内SOD的活性降低,从而引起脂质过氧化物增加来损伤多巴胺能神经细胞的。Objective:To discuss the oxidative stress damage in MPP + -induced PC12 cells,and to explore its mechanism. Methods:PC12 cells were induced by MPP + at different concentrations and intervals,cell survival rate was detected by method of MTT. cell apoptosis rate was detected by Flow cytometry,and the contents of LDH??NO??NOS??MDA and and activity of SOD were inspected by UV spectrophotometer. Results:When the concentration of MPP + reached to 300??ol/L after 48 hours,the survival rate of PC12 cells was obviously reduced,cell apoptosis rate was increased,the contents of LDH??NO??NOS??MDA and and activity of SOD were all enhanced,That was statistical significance( P 0. 05). Conclusion:The experiment certified that MPP + can induce PC12 cell oxidative stress injury,and its mechanisms maybe implement through the increasion of the leakage of LDH and increasing the contents and of NO??NOS??MDA,decreasing the activity of SOD and all the above were functioned in increasing apoptosis in PC12 cells.
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