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目的探讨氯化锰(MnCl2)对人神经细胞株PC12细胞凋亡和线粒体跨膜电位的影响,揭示锰毒性作用机制。方法取对数生长期PC12细胞,用含100、300、500、700、900μmol/LMnCl2的培养液,分别作用24、48、72h,采用四甲基偶氮唑蓝(MTT)比色实验检测细胞生长状况,流式细胞仪检测细胞凋亡和线粒体跨膜电位。结果24h后,700和900μmol/LMnCl2处理组细胞抑制率与对照组比较差异具有显著性(P<0.05);48、72h后,所有的MnCl2处理组细胞抑制率与对照组比较差异具有显著性(P<0.05);48h后,500、700和900μmol/LMnCl2处理组与对照组比较细胞G1期呈递增趋势,S期呈递减趋势,G2/M百分比和细胞凋亡率升高(P<0.05);各MnCl2处理组与对照组比较荧光强度呈不同程度下降(P<0.05)。结论MnCl2可引起PC12细胞生长抑制,导致线粒体跨膜电位下降,引起细胞凋亡。
Objective To investigate the effect of manganese chloride (MnCl2) on apoptosis and mitochondrial transmembrane potential of human neural cell line PC12 and to reveal the mechanism of manganese toxicity. Methods PC12 cells in logarithmic growth phase were treated with culture medium containing 100, 300, 500, 700 and 900 μmol / L MnCl2 for 24, 48, and 72 h, respectively. Cell viability was measured by MTT assay Growth status and flow cytometry were used to detect apoptosis and mitochondrial transmembrane potential. Results After 24 h, the inhibition rates of cells treated with 700 and 900 μmol / L MnCl2 were significantly different from those of the control group (P <0.05). After 48 and 72 h, the inhibitory rates of all cells treated with MnCl2 were significantly lower than those of the control group (P <0.05). After 48h, the cells in the 500, 700 and 900μmol / L LMnCl2 treatment groups showed an increasing trend compared with the control group, the S phase showed a decreasing trend, the G2 / M percentage and the apoptosis rate increased (P <0.05). Compared with control group, the fluorescence intensity of MnCl2 treatment group decreased to some extent (P <0.05). Conclusion MnCl2 can induce the growth inhibition of PC12 cells, resulting in the decrease of mitochondrial transmembrane potential and cell apoptosis.