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机构地区:[1]第二军医大学生理学教研室,神经科学研究所上海200433 [2]中国科学院发育生物学研究所开放实验室,北京100081
出 处:《生理学报》1998年第5期563-569,共7页Acta Physiologica Sinica
基 金:国家自然科学基金!No39330100
摘 要:本研究应用钙离子特异荧光指示剂Fura-2/AM,使用Miracal影像系统(MiracalImageSystem)检测了糖皮质激素对高钾离子升高嗜铬细胞瘤细胞(PC12细胞)内游离钙浓度([Ca2+]i)作用的影响。结果表明:(1)皮质酮抑制高钾离子诱导PC12细胞[Ca2+]i升高与其预处理细胞时间的长短有关,预处理3min时,皮质酮开始产生抑制作用;预处理5min时,其呈现的抑制作用最强;预处理25min时,抑制作用基本消失。(2)皮质酮在10-8~10-5mol/L范围内时可呈剂量-效应关系,抑制高钾离子诱导的PC12细胞[Ca2+]i升高,皮质团浓度为10-5mol/L时,其产生的抑制作用最大;在10-9mol/L时抑制作用不明显。(3)其它自体激素如皮质醇。地塞米松、孕酮、雌二醇、睾酮、醛固酮在浓度为10-5mol/L时,也能抑制高钾离子引起的PC12细胞[Ca2+]i升高,但在同一浓度时作用强度有所不同。胆固醇浓度为10-5mol/L时,对高钾离子诱导PC12细胞钙浓度升高没有抑制作用。在同一浓度时它们的作用强度顺序大致为:孕酮=皮质醇>地塞米松>睾酮>醛固酮=雌二醇>>胆固醇。(4)在皮质酮浓度为10-5mol/L时不能抑制由细胞外无钙到有钙过程引起的PC12细胞[Ca2+]i升高。The effect of glucocorticoid on the increase of cytosolic free calcium [ Ca2+ j, )induced by high-K+ was investigated in pheochomocytoma PC12 cells. The aden restiltwas as follows: (l ) When the cells were preincubated at 37t for various time intervallin the presence of 10-5 moVL of corticosterone and stimulated with 55 mrnol/L KCI, anichbitory effect of conicosterone on b [ CaZ + ]. was observed in a bine-dependent mannerwith ~rnal effect at sib adn and no effect at 25th adn. (2) adn PC12 cells werepreincubated with various concentration of corticosterone at 37T for 5 adn, the inhibitoryeffect of corticosterone on A [ Ca2+ ]. induced by 55 rnmol/L KCI was concentrationdependent. The effect was found to be maximal at 10--5 moVL of colticosternne anddiSappeared at 10-9 moUL of corticosterone. (3 ) Other steroids such as coltisol,dexalnethasone, progesterone, testosterone, 17fyeshadiol and aldosterone allo ichbitedthe rise Of [ Ca2+ ], evoked by 55 mrnoVL KCI in PC12 cells to different extents, i. e., inthe ac Of P = F > Dex > T > kid = EZ. Cholesterol was ineffetive at the concentration uptO 10-s moUL for ichbiting [ Ca2+ ], evoked by 55 nunoVL KCI. (4) Corticosteronecould not inhibit the [ Ca2+ J, rise induced by changing the concenhation of exbeellularcalcium fIDm Ca2+ -able tO 3 nimoVL.
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