TRPM2通道在星形胶质细胞氨中毒中的作用

发布时间：2018-05-14 14:40

本文选题：瞬时受体电位M阳离子通道 + 星形细胞　；参考：《中国病理生理杂志》2013年06期

【摘要】：目的:通过建立星形胶质细胞氨中毒的模型,探讨瞬时受体电位M2(TRPM2)阳离子通道在其中发挥的作用。方法:分离并培养小鼠原代星形胶质细胞。实验分为5组:对照组、氯化铵处理组、氯化铵+3-氨基苯甲酰胺(3-AB)处理组、氯化铵+PJ-34处理组和TRPM2基因敲除小鼠+氧化铵处理组。测定细胞的活性、caspase-3活性、细胞坏死和体积大小,以此来衡量氨中毒的程度。用全细胞膜片钳记录TRPM2通道电流变化。结果:氯化铵引起细胞肿胀伴随着细胞坏死。聚腺苷二磷酸核糖聚合酶(PARP)抑制剂3-AB和PJ-34抑制了氯化铵引起的阳离子电流,并减轻了氯化铵引起的相应细胞伤害。TRPM2基因敲除小鼠组细胞的伤害明显减轻(P0.01)。结论:TRMP2通道的激活是细胞暴露于氯化铵后发生肿胀、坏死的必要步骤;氯化铵诱导的星形胶质细胞肿胀与坏死密切相关。
[Abstract]:Aim: to investigate the role of transient receptor potential (M2TPM2) cationic channel in the development of astrocytic ammonia poisoning model. Methods: primary astrocytes were isolated and cultured. The experiment was divided into five groups: control group, ammonium chloride treatment group, ammonium chloride 3-aminobenzoamide 3-ABL treatment group, ammonium PJ-34 treatment group and ammonium oxide treatment group of TRPM2 gene knockout mice. The activity of caspase-3, cell necrosis and volume size were measured to measure the degree of ammonia poisoning. The current changes of TRPM2 channel were recorded by whole cell patch clamp. Results: ammonium chloride caused cell swelling and cell necrosis. 3-AB and PJ-34 inhibited the cationic current induced by ammonium chloride, and alleviated the damage of the corresponding cell injury induced by ammonium chloride. The damage of TRPM2 gene knockout mice was significantly reduced by P0.01. Conclusion the activation of the 1: TRMP2 channel is a necessary step for the swelling and necrosis of the cells after exposure to ammonium chloride, and the swelling of astrocytes induced by ammonium chloride is closely related to the necrosis.
【作者单位】：大连医科大学生理学教研室;
【基金】：国家自然科学基金资助项目(No.30971065) 大连市科技计划项目(No.2012E12SF074) 辽宁省教育厅基金资助项目(No.2009A194)
【分类号】：R363

【参考文献】