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丙磺舒可抑制胰腺β细胞中由葡萄糖刺激引起的fura-2外流。

Glucose-stimulated efflux of fura-2 in pancreatic beta-cells is prevented by probenecid.

作者信息

Arkhammar P, Nilsson T, Berggren P O

机构信息

Department of Medical Cell Biology, University of Uppsala, Sweden.

出版信息

Biochem Biophys Res Commun. 1989 Feb 28;159(1):223-8. doi: 10.1016/0006-291x(89)92426-1.

Abstract

Fura-2 loaded pancreatic beta-cells, isolated from obese hyperglycemic mice, were studied with respect to cytoplasmic free Ca2+ concentration ([Ca2+]i), insulin release and efflux of indicator. In the absence of glucose there was a continuous efflux of fura-2, which was markedly increased by stimulation with a high concentration of the sugar. Probenecid both reduced basal efflux of fura-2 and prevented that promoted by glucose. There was no interference of the drug with glucose-induced either insulin release or rise in [Ca2+]i. When applying fura-2 in pancreatic beta-cells, the use of probenecid markedly improves the measurements of [Ca2+]i.

摘要

研究了从肥胖高血糖小鼠分离出的负载有Fura-2的胰腺β细胞的细胞质游离钙离子浓度([Ca2+]i)、胰岛素释放及指示剂流出情况。在无葡萄糖情况下,Fura-2持续流出,高浓度糖刺激可使其显著增加。丙磺舒既降低了Fura-2的基础流出量,又阻止了葡萄糖促进的流出。该药物对葡萄糖诱导的胰岛素释放或[Ca2+]i升高无干扰。在胰腺β细胞中应用Fura-2时,丙磺舒的使用显著改善了[Ca2+]i的测量。

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