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机构地区:[1]中国医科大学神经生物学教研室,辽宁沈阳110001
出 处:《解剖科学进展》2007年第3期193-195,199,共4页Progress of Anatomical Sciences
基 金:国家自然科学基金(30400145;30600060;30570650);辽宁省自然科学基金(20052102);博士学科点专项科研基金(20050159005)
摘 要:目的探讨缓激肽持续作用引起的胶质瘤细胞内钙离子浓度变化([Ca2+]i)及机制。方法培养大鼠C6胶质瘤细胞,采用[Ca2+]i测定和免疫荧光细胞化学鉴定的方法,观察持续给予缓激肽后胶质瘤细胞内[Ca2+]i的变化和缓激肽B2受体在细胞内的分布。结果在第一次给予缓激肽时,引起[Ca2+]i的峰值最大,随着给予缓激肽次数的增加,缓激肽诱导的[Ca2+]i荧光强度峰值逐渐下降,在第5次加入缓激肽时,[Ca2+]i荧光强度峰值已无显著变化。在此过程中,缓激肽B2受体发生内化,并与胞浆中的质膜微囊蛋白caveolin-1结合。结论持续给予缓激肽可引起胶质瘤细胞内[Ca2+]i浓度规律变化,caveolin-1可能参与此过程。Objective To study the [Ca^2+]i change and mechanism induced by continuous stimulation of bradykinin in glioma cells. Methods [Ca^2+]i assay and immunofluorescence staining were used to observe the [Ca^2+]i change and the location of bradykinin B2 receptors after the continuous treatment with bradykinin in cultured rat C6 glioma cells. Results With the first stimulation of bradykinin, [Ca^2+]i fluorescence intensity ascends to peak and descends gradually as the continuous stimulation of bradykinin, and with no significant change of [Ca^2+]i fluorescence intensity at the fifth stimulation. During this process, combination of bradykinin B2 receptors with caveolin-1 was observed in cytoplasma. Conclusions Continuous administration of bradykinin can cause the regular change of [Ca^2+]i concentration in glioma, in which caveolin-1 may be involved.
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