MPP+和6-羟基多巴胺对C6胶质瘤细胞摄取谷氨酸的影响1

目的 研究1-甲基-4-苯基-吡啶离子(MPP⁺)6-羟基多巴胺(6-OHDA)对C6 胶质瘤细胞摄取谷氨酸(Glu)的影响。方法 应用放射免疫法测定C6胶质瘤细胞对培养液中[³H] -D,L-谷氨酸的摄取;应用四氮唑(MTT)比色法检测胶质瘤细胞的活性。结果 6-OHDA 和MPP⁺均不同程度地抑制C6 胶质瘤细胞摄取Glu;6-OHDA 显著抑制C6 胶质瘤细胞活性,而MPP⁺却不影响细胞活性;蛋白激酶C(PKC)激动剂TPA 显著增强C6 细胞对Glu 的摄取,并拮抗MPP⁺对C6 细胞摄取Glu 的抑制。结论 6-OHDA 抑制C6 胶质瘤细胞对Glu 的摄取,可能与其抑制细胞活性有关,而MPP⁺的抑制作用可能与直接影响转运体的摄取功能有关,并可能由PKC 途径介导。

Effects of 1-methy-4-phenylpyridinium and 6-hydroxydopamine on the glutamate uptake into cultured C6 glioma cells1

AIM: To study the effects of 6-OHDA and MPP⁺on the glutamate uptake into cultured C6 glioma cells.METHODS: The glutamate uptake into C6 glioma cells was measured by using radioimmunoassay method;and the viability of C6 glioma cells was investigated by MTT method.RESULTS: Both 6-OHDA and MPP⁺inhibited glutamate uptake into C6 glioma cells in a concentration-dependent manner.Treatment with 6-OHDA produced inhibitory effect on the viability of C6 glioma cells.However,exposure to MPP⁺showed no such effect.Incubation with TPA,a PKC activator,caused increase in glutamate uptake and completely reversed MPP⁺-induced uptake inhibition.CONCLUSION: Inhibition of glutamate uptake by MPP⁺was completely reversed by TPA,indicating that the effect of MPP⁺was mediated by PKC cell signal transduction,while the inhibitory effect of 6-OHDA was due to the impairment viability of C6 glioma cells.