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作 者:虞涛[1] 贺军[2] 胡萍[1] 陈群力[3] 邵静芳[1] 杨敬[1] 沈关心[1] 龚非力[1]
机构地区:[1]华中科技大学同济医学院免疫学系,武汉430030 [2]华中科技大学生命与科学技术学院光子所 [3]河南科技大学生物化学教研室
出 处:《中华内分泌代谢杂志》2005年第4期369-372,共4页Chinese Journal of Endocrinology and Metabolism
基 金:国家自然科学基金资助项目(No.30300166)
摘 要:目的研究K+通道阻断剂四乙胺(TEA)对胰岛β细胞凋亡的影响。方法以γ干扰素(IFNγ)+白细胞介素1β(IL1β)或链脲佐菌素(STZ)作用于小鼠胰岛细胞(NIT细胞),同时加入TEA,通过AnnexinV碘化丙啶(PI)、PI、Rhodamine123染色,采用流式细胞仪检测细胞凋亡与细胞膜电势;用MTT法检测细胞活性。结果IFNγ+IL1β或STZ可明显诱导NIT细胞凋亡,诱导组细胞存活率、凋亡率与未诱导组及TEA组差异均有统计学意义(均P<0.01);TEA能抑制诱导的NIT细胞凋亡(均P<0.01)。结论胰岛β细胞凋亡过程中可能也存在K+外流现象,K+通道在胰岛β细胞的凋亡中可能起着重要作用;TEA可抑制凋亡刺激剂诱导的胰岛β细胞凋亡,其效应可能与阻止K+外流有关。Objective To study the effect of tetraethylammonium (TEA, K^+ channel blocker) on mouse islet β-cell apoptosis. Methods Mouse β cells ( NIT cells) were exposed to interferon-γ( IFN-γ ) + intedeukin-1β(IL-1β) or streptozotocin (STZ) to induce cell apoptosis, and TEA was added along with apoptotic insults to prevent the efflux of intracellular K^+. Cells were stained with annexin V-propidium iodine (PI) , PI and rhodamine123; flowcytometer (FCM) was used to detect the apoptosis of NIT cells and change in mitochondrial membrane potential. MTT was used to observe the effect of TEA on the viability of NIT Cells. Results IFN-γ+IL-1β or STZ significantly induced the apoptosis of NIT cells (both P〈0.01) and TEA obviously inhibited the apoptosis of NIT cells induced by both stimuli ( both P〈0.01 ). Conclusion The efflux of intracellular K^+ occurs probably during apoptosis of islet β-cells, which may be related to activation of K^+ channels. TEA may inhibit the apoptosis of islet β-cells by blocking the efflux of K^+.
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