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磷脂酶A2诱导的大鼠胸膜炎症

Phospholipase A2-induced pleural inflammation in rats.

作者信息

Weichman B M, Berkenkopf J W, Marshall L A

机构信息

Division of Immunopharmacology, Wyeth-Ayerst Research, Princeton, NJ 08543.

出版信息

Int J Tissue React. 1989;11(3):129-36.

PMID:2533186
Abstract

Injection of Naja mocambique mocambique phospholipase A2 [PLA2] into the rat pleural cavity induced dose- and time-dependent fluid accumulation and cellular infiltration. The time course of the cell influx was initially neutrophilic [2-6 h] and later mononuclear [6-24 h]. During reverse passive Arthus reaction [RPAR] induced pleurisy, endogenously produced PLA2 activity, quantitated by the hydrolysis of [3H]-arachidonic acid E. coli substrate, was detected in the pleural exudate. However, the biosynthesis of eicosanoids and plasma extravasation in the pleural cavity preceded the 9-fold elevation in PLA2 activity which was obtained at 4 h. Whereas the exact role of PLA2 in the inflammatory response remains to be determined, these results demonstrate that exogenous PLA2 can induce pleural inflammation in the rat, and that this enzyme is released endogenously during experimental pleurisy.

摘要

将莫桑比克射毒眼镜蛇磷脂酶A2 [PLA2] 注入大鼠胸腔会引起剂量和时间依赖性的液体蓄积及细胞浸润。细胞流入的时间进程最初是嗜中性的 [2 - 6小时],随后是单核的 [6 - 24小时]。在反向被动阿瑟斯反应 [RPAR] 诱导的胸膜炎中,通过 [3H]-花生四烯酸大肠杆菌底物的水解定量检测到胸膜渗出液中内源性产生的PLA2活性。然而,在4小时时PLA2活性升高9倍之前,胸腔中类花生酸的生物合成和血浆外渗就已经发生。虽然PLA2在炎症反应中的确切作用仍有待确定,但这些结果表明外源性PLA2可诱导大鼠胸膜炎症,并且在实验性胸膜炎期间该酶会内源性释放。

相似文献

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Phospholipase A2-induced pleural inflammation in rats.磷脂酶A2诱导的大鼠胸膜炎症
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2
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