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目的观察醒脑静注射液对Aβ25-35诱导的SH-SY5Y细胞线粒体损伤的保护作用。方法将培养的SH-SY5Y细胞随机分为5组,即(1)正常对照组:细胞正常培养27 h;(2)AD细胞模型组:细胞正常培养3 h,随后用老化的Aβ25-35(25μmol/L)处理24 h;(3)醒脑静低浓度组:醒脑静注射液(5μl/m L)预处理细胞3h,随后用老化的Aβ25-35(25μmol/L)处理24 h;(4)醒脑静中浓度组:醒脑静注射液(10μl/m L)预处理细胞3h,随后用老化的Aβ25-35(25μmol/L)处理24 h;(5)醒脑静高浓度组:醒脑静注射液(20μl/m L)预处理细胞3h,随后用老化的Aβ25-35(25μmol/L)处理24 h;处理后各组细胞利用MTT法检测细胞存活率,紫外分光光度法检测细胞内ATP含量,流式细胞仪检测线粒体膜电位水平。结果 AD细胞模型组细胞存活率较正常对照组降低(P<0.05),醒脑静不同浓度组细胞存活率较AD细胞模型组均明显升高(P<0.05);AD细胞模型组细胞内ATP含量、线粒体膜电位水平较正常对照组下降(P<0.05),醒脑静不同浓度组细胞内ATP含量、线粒体膜电位水平较AD细胞模型组显著升高(P<0.05)。结论醒脑静预处理可抑制Aβ25-35诱导的SH-SY5Y细胞凋亡,提高细胞存活率,其机制可能与醒脑静提高细胞内ATP含量及线粒体膜电位水平而发挥线粒体保护作用有关。
Objective To observe the protective effects of xingnaojing injection on Aβ25-35 induced mitochondrial damage in SH-SY5Y cells. Methods The cultured SH-SY5Y cells were randomly divided into 5 groups: (1) normal control group: normal cultured cells for 27 h; (2) AD cell model group: normal cultured cells for 3 h, then treated with aging Aβ25-35 25μmol / L) for 24 h. (3) Xingnaojing low concentration group: Xingnaojing injection (5μl / m L) pretreated cells for 3h, then treated with Aβ25-35 (25μmol / L) (4) Concentration group of Xingnaojing injection: Xingnaojing injection (10μl / ml) pretreated cells for 3h, then treated with Aβ25-35 (25μmol / L) for 24 hours; (5) The cells were pretreated with xingnaojing injection (20μl / m L) for 3h and then treated with Aβ25-35 (25μmol / L) for 24 hours. After treatment, the cell viability was measured by MTT assay and the UV spectrophotometry Method to detect intracellular ATP content, flow cytometry detection of mitochondrial membrane potential. Results The survival rate of cells in AD model group was lower than that in normal control group (P <0.05), and the survival rate of cells in different concentrations of Xingnaojing group was significantly higher than that in AD model group (P <0.05) (P <0.05). The contents of ATP and mitochondrial membrane potential in Xingnaojing group were significantly higher than those in AD model group (P <0.05). Conclusion Xingnaojing pretreatment can inhibit the apoptosis of SH-SY5Y cells induced by Aβ25-35 and improve the cell survival rate. The mechanism may be related to the action of Xingnaojing on increasing intracellular ATP content and mitochondrial membrane potential.