Nakano T, Arita H
Shionogi Research Laboratories, Shionogi & Co. Ltd., Osaka, Japan.
FEBS Lett. 1990 Oct 29;273(1-2):23-6. doi: 10.1016/0014-5793(90)81042-m.
We studied the regulation of group II phospholipase A2 (PLA2-II) gene in vivo, using endotoxin shock rat as a model for systemic inflammation. Administration of endotoxin into rats increased PLA2 activity in the plasma, as described by Vadas and Hay, using endotoxin-challenged rabbit. Specific absorption of this activity by anti-PLA2-II antibody indicated that the released PLA2 was PLA2-II. The levels of PLA2-II mRNA were elevated in the aorta, spleen, lung, and thymus but not in the liver and kidney. The tissues with high PLA2-II mRNA contents released a greater amount of PLA2-II than the tissues of control rats. These results suggest that in endotoxin shock rats, PLA2-II is synthesized de novo in the above tissues and released into circulation. Furthermore, our present study demonstrates that glucocorticoid suppresses the enhanced expression of the PLA2-II gene in the tissues of endotoxin shock rats.
我们以内毒素休克大鼠作为全身炎症的模型,在体内研究了II型磷脂酶A2(PLA2-II)基因的调控。如Vadas和Hay利用内毒素攻击的兔子所描述的那样,给大鼠注射内毒素会增加血浆中的PLA2活性。抗PLA2-II抗体对该活性的特异性吸收表明,释放的PLA2是PLA2-II。PLA2-II mRNA水平在主动脉、脾脏、肺和胸腺中升高,但在肝脏和肾脏中未升高。与对照大鼠的组织相比,具有高PLA2-II mRNA含量的组织释放出更多的PLA2-II。这些结果表明,在内毒素休克大鼠中,PLA2-II在上述组织中重新合成并释放到循环中。此外,我们目前的研究表明,糖皮质激素可抑制内毒素休克大鼠组织中PLA2-II基因的增强表达。