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采用四唑盐比色、琼脂糖凝胶电泳、乙二酸荧光素染色和Hoechst332 58染色等方法研究高钾对原代培养的大鼠小脑颗粒神经元的毒性作用及其机制。结果发现 :①高钾诱导神经元死亡呈剂量 ( 50～ 10 0mmol/L)和时间依赖性 ;②神经元死亡呈现明显的凋亡特征 :胞体缩小 ,染色质浓缩 ,DNA“梯形”条带形成和蛋白质合成抑制剂 (cycloheximide ,1.0mg/L)可阻断其毒性等 ;③MK 80 1( 2 μmol/L)、尼莫地平 ( 10 μmol/L)、硫酸镁 ( 2 0mmol/L)可阻断高钾的大部分毒性作用。结果提示 :高钾可能通过刺激内源性谷氨酸释放从而诱导小脑颗粒神经元凋亡
The toxic effects of high potassium on primary cultured rat cerebellar granule neurons and its mechanism were studied by tetrazolium salt colorimetric, agarose gel electrophoresis, fluorescein oxalate staining and Hoechst332 58 staining. The results showed that: (1) high potassium induced neuronal death in a dose (50 ~ 100mmol / L) and time-dependent manner; (2) neuronal death showed obvious apoptotic features: cell body shrinkage, chromatin condensation, DNA “trapezoidal” And cycloheximide (1.0 mg / L) blocked its toxicity. ③MK 80 1 (2 μmol / L), nimodipine (10 μmol / L) and magnesium sulfate Most of the high potassium potassium toxicity. The results suggest that high potassium may induce cerebellar granule neuron apoptosis by stimulating the release of endogenous glutamate