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机构地区:[1]中国医学科学院基础医学研究所
出 处:《中国医学科学院学报》1993年第3期168-171,共4页Acta Academiae Medicinae Sinicae
摘 要:在NG108-15细胞株上,用荧光探针fura-2/AM测定细胞内游离钙([Ca^(2+)]1)浓度。结果表明:丁二酰cAMP(Bt_2cAMP)、腺苷酸环化酶激动剂forskolin和蛋白激酶C激动剂十四碳酰佛波醇酯(TPA)均能使([Ca^(2+)]i)升高。钙通道拮抗剂异搏定(verapamil)可以抑制forskolin、Bt_2cAMP和TPA引起的[Ca^(2+)]i增加。δ阿片受体激动剂[D-Pen^2,D-Pen^5)enkephalin(DPDPE)能抑制Bt_2cAMP和forskolin引起的[Ca^(2+)]i增加,但不影响TPA引起的[Ca^(2+)]i增加。提示DPDPE可抑制cAMP依赖的蛋白激酶引起的钙内流,而与蛋白激酶C(PKC)引起的钙内流无关。The effect of DPDPE on intracelluar free calcium concentration in neu-roblastoma glioma hybrid cells(NG108-15) was studied with fura-2/AM floure-scence. The results were as follows:1) The membrane permeable cAMP anologue Bt2cAMP, the adenylate cyclase activator forskolin and the protein kinase C activator TPA all induced an increase in intracelluar free calcium concentration. 2) Verapamil suppressed the increase of [Ca2+]i induced by Bt2cAMP, forskolin and TPA. 3) DPDPE blocked the increase of [Ca2+]i induced by Bt2cAMP and forskolin, but not that induced by TPA. These results imply that DPDPE suppresses cyclic AMP-dependent protein kinase-induced but not protein kinase C-induced intracellular free calcium.
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