摘要
目的 :分析皮质酮快速抑制高钾诱导PC12细胞内钙升高的机制。方法 :使用荧光影像系统 ,实时检测细胞内钙变化。结果 :①在预处理PC12细胞 5min后 ,皮质酮可呈量 -效关系抑制高钾诱导的PC12细胞内钙升高。②牛血清白蛋白耦联的皮质酮 (B BSA)可模拟皮质酮快速抑制高钾诱导PC12细胞内钙升高的作用 ,并呈现量 -效关系。③糖皮质激素的细胞内受体拮抗剂RU38486对皮质酮快速抑制效应无明显拮抗作用。④蛋白合成抑制剂放线菌酮预处理细胞 3h后 ,皮质酮对高钾诱导PC12内钙升高仍有较强抑制作用。结论 :①皮质酮的作用点位于细胞膜上。②皮质酮的快速作用不直接依赖细胞内蛋白合成和不依赖细胞内糖皮质激素受体。
Aim: To analyse the mechanism of corticosterone on the elevation of cytosolic free calcium (i) induced by high-K + in pheochromocytoma PC12 cells, Methods: The i was real-time checked by fluorescenc image system.Results: ①When the cells were preincubated at 37℃ for 5 min in the presence of various concentration corticosterone and stimulated with 55 mmol/L KCl , an inhibitory effect of corticosterone on Δi was observed in a concentration-dependent manner. ② When PC12 cells were preincubated with various concentration of B-BSA at 37℃ for 5 min and stimulated with 55 mmol/L KCl, an inhibitory effect of B-BSA on Δi was observed, which is also concentration-dependent manner. ③ The inhibitory effect of corticosterone and B-BSA could not be antagonized by RU 38486 at 10 -4 mol/L. ④cycloheximide could not block the inhibitory effect of corticosterone after pretreating cells at 10 -5mol/L at 37℃ for 3 hours. Conclusion: It is obvious that the locus of corticosterone action is on the plasmic membrane. The inhibitory effect of corticosterone is independent of protein synthesis and intracelullar glucocorticoid receptor. The effect of corticosterone on i is nongenomic action in PC12 cells.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2002年第1期47-50,共4页
Chinese Journal of Applied Physiology
基金
中科院生理所神经科学开放实验室 ( 0 10 111)
国家自然科学基金资助项目 ( 139930 0 80 )
