摘要
目的:通过铝对大鼠脑细胞内三磷酸肌醇(IP3)合成的影响,探讨铝的神经毒性机制。方法:取摄用含Al2(SP4)32.5%饮水6个月大鼠及未摄铝同龄对照组大鼠大脑皮质,以AmershamIP3测试系统测定各组脑组织IP3含量并观察M受体激动剂carbachol及KCl(40mM)对IP3合成的影响。结果:摄铝大鼠脑组织基础IP3含量明显低于对照组(P<0.01),铝抑制carbachol及K+诱发的IP3的合成(P<0.01)。结论:高浓度铝降低基础IP3的含量,并抑制carbachol及K诱发的IP3的生物合成。抑制G蛋白磷脂酶C偶连及IP2敏感的磷脂酶C为铝对脑细胞毒性的机制之一。
Objective: : To study the neurotoxic mechanism of aluminum based on the metabolic changes of phos-phoinositide. Methods: Adult experimental rats drank water with 2. 5% Al2 (SO4 )3 while control drank water with the same pH as experimental group but without Al2(SO4)3 for 6 months . Amersham IP3 assay system was used to measure IP3 of brain tissue from all groups and the effects of carbachol, KC1 (40mM) on the synthesis of IP3 were examined as well. Results: the basal IP3 of brain tissues treated with aluminum was significantly lower than that of control (P<0. 01) , aluminum inhibited carbachol and K+ -induced synthesis of IP3 (P<0. 01). Conclusions: aluminum reduce basal IP3 and inhibit carbachol and K+ -induced synthesis of IP3. The mechanism of inhibition by aluminum is by damage of the linkage between G protein and phospholipase C and the IP2-sensitive phospholipase C.
出处
《脑与神经疾病杂志》
2005年第1期35-36,共2页
Journal of Brain and Nervous Diseases
关键词
铝
三磷酸肌醇
脑细胞
大鼠
aluminum inositol trisphosphate(IP3) [Ca2+]i brain rats
