氯化锰对PC12细胞凋亡和线粒体跨膜电位的影响

Effect of manganese chloride on PC12 apoptosis and transmitochondrial membrane potential

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 research the toxic effects on manganese chloride（MnCl2） of apoptosis and mitochondrial transmembrane potential of pheochromocytoma （PC12） cells and to reveal the molecular mechanisms of dysfunction caused by manganese. Methods PC12 cells in logarithm period were incubated in culture media of MnC12 at 100,300,500,700,900 μmol/L for 24,48 and 72 hours respectively, cell viability was examined by MTT. Cell cycle, apoptosis and mitochondrial transmembrane potential were monitored by flow cytometry （FCM）. Results Compared with the control group,24 hours after the incubation, the cell inhibition rates only in 700 and 900 μmol/L MnC12 groups were significantly increased （ P 〈 0.05 ）, while at 48 and 72 hours, cells inhibition rates at every MnC12 group were significantly increased （P 〈 0. 05）. At 48 hours, the results of 500,700 and 900 μmol/L MnC12 group showed that, compared with the control group, G1 phase was increased, S phase was decreased,the percentage of G2/M and apoptosis were increased （ P 〈 0. 05 ） respectively. The cell membrane potential was decreased compared with control group. Conclusion MnC12 could bring down mitochondrial transmembrane potential of PC12 cells and inhibit multiplication of cells and induce cell apoptosis.