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环氧化酶抑制剂可减弱终板血管器中谷氨酸释放增加以及葡萄球菌肠毒素A诱导的发热。

Cyclooxygenase inhibitors attenuate augmented glutamate release in organum vasculosum laminae terminalis and fever induced by staphylococcal enterotoxin A.

作者信息

Huang Wu-Tein, Wang Jhi-Joung, Lin Mao-Tsun

机构信息

Department of Health Care Administration, Di Wan College of Management, Tainan, Taiwan.

出版信息

J Pharmacol Sci. 2004 Feb;94(2):192-6. doi: 10.1254/jphs.94.192.

Abstract

Both the hyperthermia and augmented glutamate release in the organum vasculosum laminae terminalis (OVLT) after an intravenous dose (30 ng/kg) of staphylococcal enterotoxin A (SEA) were significantly reduced by pretreatment with intravenous administration of cyclooxygenase inhibitors such as aspirin (1 - 10 mg/kg), sodium salicylate (1 - 10 mg/kg), or diclofenac (10 mg/kg). Intra-OVLT administration of 50 - 200 microg in 1.0 microl of either aspirin or sodium salicylate 60 min before or 120 min after an intra-OVLT dose (50 microg in 1.0 microl) of glutamate also significantly suppressed the glutamate-induced hyperthermia. These findings suggest that inhibition of cyclooxygenase receptor mechanisms suppresses SEA fever by inhibition of glutamate release in the OVLT of rabbit brain.

摘要

静脉注射剂量为30 ng/kg的葡萄球菌肠毒素A(SEA)后,终板血管器(OVLT)中的体温过高和谷氨酸释放增加的情况,通过静脉注射环氧合酶抑制剂如阿司匹林(1 - 10 mg/kg)、水杨酸钠(1 - 10 mg/kg)或双氯芬酸(10 mg/kg)进行预处理后均显著降低。在OVLT内注射谷氨酸剂量(1.0微升中含50微克)前60分钟或后120分钟,在1.0微升中注射50 - 200微克的阿司匹林或水杨酸钠,也显著抑制了谷氨酸诱导的体温过高。这些发现表明,环氧合酶受体机制的抑制通过抑制兔脑OVLT中的谷氨酸释放来抑制SEA发热。

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