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用凝胶电泳和 fura- 2荧光技术测定 [Ca2 + ]i方法研究咖啡因对低钾诱导的大鼠小脑颗粒神经元凋亡的保护作用与 [Ca2 + ]i 升高之间的关系 .将体外培养的小脑颗粒神经元从高钾 ( 2 5mmol· L-1KCl)培养基中转移到低钾 ( 5mmol· L-1KCl)培养基中 ,神经元发生凋亡 .但低钾引起的神经元死亡可被咖啡因 ( 5- 2 0 mmol· L-1)浓度依赖性地保护 ,且咖啡因的这种作用不受蓝尼定 ( ryanodine) -敏感钙释放阻断剂蓝尼定和丹曲林 ( dantrolene)的影响 ;也不被 L-型钙通道阻断剂硝苯地平 ,尼莫地平 ,维拉帕米和 NMDA受体阻断剂地佐环平抑制 .结果说明 [Ca2 + ]i 的升高并不是咖啡因对小脑颗粒神经元的保护作用所必需的 .
The relationship between [Ca2 +] i and caffeine on the apoptosis of cerebellar granule neurons induced by hypokalemia in rats was investigated by gel electrophoresis and fura-2 fluorescence assay. In vitro cultured cerebellar granule neurons were transferred from high potassium (25 mmol · L-1 KCl) medium to low potassium (5 mmol · L-1 KCl) medium, neurons apoptosis, but hypokalemia-induced neuronal death Can be concentration-dependently protected by caffeine (5-20 mmol · L -1), and this effect of caffeine is not inhibited by the ryanodine-sensitive calcium release blockers, (dantrolene), and was not inhibited by L-type calcium channel blockers nifedipine, nimodipine, verapamil and NMDA receptor antagonist zorbazepine.The results showed that [Ca2 +] i Elevation is not necessary for protection of cerebellar granule neurons by caffeine.