肿瘤坏死因子-α激活ECV304钙激活钾通道及G蛋白的增强效应  

G-protein Potentiates the Activation of TNF-α on Calcium-activated Potassium Channel in ECV304

作　　者：林琳[1] 郑永芳[1] 屈金河[1] 鲍光宏[1] 

机构地区：[1]中国医学科学院中国协和医科大学基础医学研究所生理研究室,北京100005

出　　处：《中国医学科学院学报》2000年第3期232-236,共5页Acta Academiae Medicinae Sinicae

基　　金：国家自然科学基金重点项目!(39730 2 2 0 )

摘　　要：目的　观察肿瘤坏死因子 -α(TNF-α)对人脐静脉内皮细胞株 ECV30 4钙激活钾通道 (BKca)的影响以及 G蛋白是否在此过程中起作用。方法　细胞贴附式膜片箝技术。结果　发现 ECV30 4细胞膜上存在大电导钙激活钾通道 (BKca) ,它的电导是 (2 0 2 .5 4± 16 .6 2 ) p S,其活动可被 2 0 0 U / m l TNF-α增强 ,G蛋白在此过程中起介导作用。结论　 TNF-α作用于内皮细胞 ,快速激活 BKca,促进钾离子大量外流 ,使细胞膜发生超极化 ,增大静息钙离子内流的电化学驱动力 ,开放静息钙通道升高静息胞内钙离子浓度。G蛋白可增强此激活效应。Observe the effect of tumor necrosis factor-α(TNF-α) on calcium-activated potassium channel in ECV304 and the possible involvement of G-protein mediation in the action of TNF-α. Method Using the cell-attached configuration of patch clamp technique. Results (1)the activity of highconductance calcium-actiated potassium channel (BKc a) was recorded.Its conductance is (202.54±16.62) pS;(2)the activity of BKc a was potentiated by 200U/ml TNF-α;(3)G-protein would intensify this TNF-α activation. Conclusions TNF-α acted on vascular endothelial cell ECV304 could rapidly activate the activity of BKc a.Opening of BKc a resulted in membrane hyperporlarization which could increase electro-chemical gradient for the resting Ca 2+influx and open leakage calcium channel,thus resting cytoplasmic free Ca 2+concentration could be elevated.G-protein may exert an important regulation in this process.

关 键 词：钙激活钾通道 肿瘤坏死因子-Α G蛋白 增强效应 

分 类 号：R322.123[医药卫生—人体解剖和组织胚胎学] R329.25[医药卫生—基础医学]