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刺激甲状腺磷脂释放花生四烯酸。

Stimulation of arachidonic acid release from thyroid phospholipids.

作者信息

Stelmach H, Jaroszewicz L

机构信息

Department of Physical Chemistry, Medical Academy of Białystok, Poland.

出版信息

J Physiol Pharmacol. 1995 Dec;46(4):439-46.

PMID:8770788
Abstract

The present study demonstrates that exposure of pig thyroid slices to thyrotropin stimulates the arachidonate release from endogenous phospholipids. The experiments with 14C-arachidonic acid show that the release of arachidonic acid is mostly from phosphatidylcholine, phosphatidylinositol and neutral lipids. The liberation of arachidonate from thyroid phospholipids is Ca2+ dependent. The addition of calcium ionophore A23187 to medium augments the release of arachidonate. Addition of ionophore and egzogenous Ca2+ markedly stimulates the arachidonate release, what suggests that thyroid phospholipase A2 can be regulated by the extend of saturation of the enzyme with Ca2+. The arachidonate release from phospholipids caused by thyrotropin is potentiated by adenosine. This effect shows that adenosine modulates TSH action and supports the idea that adenosine takes part in the physiological regulation of thyroid cells.

摘要

本研究表明,将猪甲状腺切片暴露于促甲状腺激素会刺激花生四烯酸从内源性磷脂中释放出来。用14C-花生四烯酸进行的实验表明,花生四烯酸的释放主要来自磷脂酰胆碱、磷脂酰肌醇和中性脂质。甲状腺磷脂中花生四烯酸的释放依赖于Ca2+。向培养基中添加钙离子载体A23187可增加花生四烯酸的释放。添加离子载体和外源性Ca2+可显著刺激花生四烯酸的释放,这表明甲状腺磷脂酶A2可受该酶Ca2+饱和程度的调节。促甲状腺激素引起的磷脂中花生四烯酸的释放可被腺苷增强。这一效应表明腺苷可调节促甲状腺激素的作用,并支持腺苷参与甲状腺细胞生理调节的观点。

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