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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。③皮质酮对高钾诱导PC12内钙升高的快速抑制作用属非基因组作用
OBJECTIVE: To analyze the mechanism of cortisone rapidly inhibiting hypercalcemia-induced increase of intracellular calcium in PC12 cells. Methods: Fluorescence imaging system was used to detect intracellular calcium changes in real time. Results: (1) After pretreatment of PC12 cells for 5 minutes, corticosterone inhibited the hypercalcemia-induced increase of intracellular calcium in PC12 cells in a dose-effect relationship. ② Bovine serum albumin-linked corticosterone (B BSA) could mimic the effect of corticosterone on the rapid calcium-induced increase of intracellular calcium in PC12 cells with dose-effect relationship. ③ glucocorticoid receptor antagonist RU38486 intracellular corticosterone rapid inhibitory effect no significant antagonism. ④ protein synthesis inhibitor cycloheximide pretreatment cells 3h, corticosterone on high potassium-induced increase in PC12 calcium still strong inhibitory effect. Conclusion: ① The role of corticosterone in the cell membrane. The rapid effects of corticosterone do not directly depend on intracellular protein synthesis and do not rely on intracellular glucocorticoid receptors. ③ corticosterone on high potassium-induced rapid increase in PC12 calcium inhibition is a non-genomic effect