中文摘要：

目的：研究急性冠状动脉综合征（ACS）患者外周血中CD4＋T细胞及CD4＋CD28null亚型活化前后IKCal钾通道数目的变化以及IKCal钾通道阻滞剂对活化CD4＋T细胞效应分子表达的影响，探讨IKCal钾通道对不稳定斑块的意义。方法：用免疫磁珠法分离出24例ACS患者外周血中的CD4＋T细胞，其中12例进一步分出亚型CD4＋CD28nullT细胞，采用全细胞膜片钳技术记录细胞活化前及活化3d后的IKCal钾电流。CD4＋T细胞活化3d后分别加入终浓度为0．2、1、5μmol／L特异性IKCal钾通道阻滞剂TRAM-34，再继续活化3d，用反转录-PCR法检测干扰素-γ及颗粒酶BmRNA的表达。结果：活化后CD4＋、CD4＋CD28nullT细胞的IKCal通道数目分别增加了9倍和8倍[活化前后2种细胞的通道数分别为（45±3）：（439±33），（56±4）：（497±45），均P〈0．01]。2种细胞的通道密度也分别增加了约3倍（P〈0．01）。活化前及活化后2种细胞的通道数目及通道密度均无差别。不同浓度的TRAM-34均下调CD4＋T细胞活化后干扰素-γ、颗粒酶BmRNA的表达，各浓度组间干扰素-γ、颗粒酶BmRNA的表达差异均有统计学意义（P〈0．01），浓度越高，各mRNA表达越低。结论：ACS患者外周血CD4＋及CD4＋CD28nullT细胞活化后IKCal的通道数目及通道密度均明显增加，特异性IKCal通道阻滞剂TRAM-34呈浓度依赖性地抑制CD4＋T细胞活化时干扰素-γ及颗粒酶BmRNA的表达，提示CD4＋T细胞的IKCal钾通道可作为预防动脉粥样斑块不稳定的潜在治疗靶点。

英文摘要：

Objective： To study the number changes of IKCal channel during activation on peripheral blood CD4＋ T cells and its subset CD4＋ CD28null in acute coronary syndrome（ACS） patients and the effects of IKCal-specific channel blocker on effectors expression of activated CD4＋ T cell , further discuss the implication of IKCal channel for unstable plaque. Methods：CD4＋ T cell in all of and CD4＋ CD28nullT cells in 12 of 24 ACS patients were isolated from peripheral blood through magnetic ceil sorting. The whole cell IKCal currents of T ceils above were recorded with patch-clamp technique before and 3 days after activation by purified anti-human CD3. 0.2, 1, 5μM of TRAM-34, a specific blocker of IKCal channel, were added respectively to CD4＋T cell after 3-day activation, then another 3 days activation, and Interferon gamma, Granzyme B mRNA expression of CD4＋ T cell were determined by reverse transcription-PCR. Results：IKCal channels per cell on activated CD4＋T cell were 9 times higher than those on resting CD4＋T cell, and on activated CD4＋CD28nullT cell 8 times higher （439±33 vs. 45±3, 497±45 vs. 56±4 channels per cell after vs. before activation respectively, both P〈0.05）. Both activated T cells had up to triple channel density, compared to their resting ones（both P〈0.05）. The numbers and density of IKCal channel were parallel between both T cells regardless of activation. The mRNA expression of Interferon gamma and Granzyme B were down-regulated by all μM of TRAM-34, and differential expression of each mRNA existed among variedμM of TRAM-34 （P〈0.01, respectively）. The largerμM of TRAM-34, the smaller expression of each mRNA. Conclusions： IKCal channels increase substantially on peripheral blood CD4＋T cell and its subset CD4＋ CD28nullT cell after activation in ACS patients, and IKCal-specific channel blocker TRAM-34 can inhibit the mRNA expression of Interferon gamma and Granzyme B in CD4＋ T cell in a dose-depend pattern. Hence, IKCal channel on CD4＋T cell may