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首页> 外文期刊>Journal of pharmacological sciences. >Lipopolysaccharide- and glutamate-induced hypothalamic hydroxyl radical elevation and fever can be suppressed by N-methyl-D-aspartate-receptor antagonists.
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Lipopolysaccharide- and glutamate-induced hypothalamic hydroxyl radical elevation and fever can be suppressed by N-methyl-D-aspartate-receptor antagonists.

机译：N-甲基-D-天冬氨酸受体拮抗剂可以抑制脂多糖和谷氨酸诱导的下丘脑羟基自由基升高和发热。

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摘要

The purpose of the current study was to explore the effects of N-methyl-D-aspartate (NMDA)-receptor antagonists (MK-801 and LY235959) administered intracerebroventricularly on the changes of both core temperature and hypothalamic levels of 2,3-dihydroxybenzoic acid (2,3-DHBA) induced by intracerebroventricular injection of glutamate (100 - 400 microg at 10 microl/rabbit) or intravenous administration of lipopolysaccharide (LPS) (2 microg/kg) in rabbits. The measurements of 2,3-DHBA were used as an index of the intrahypothalamic levels of hydroxyl radicals. The rise in both the core temperature and hypothalamic 2,3-DHBA could be induced by intracerebroventricular injection of glutamate or intravenous administration of LPS. The glutamate- or LPS-induced fever and increased hypothalamic levels of 2,3-DHBA were significantly antagonized by pretreatment with injection of MK-801 or LY235959 1 h before glutamate or LPS injection. The increased levels of prostaglandin E2 in the hypothalamus induced by glutamate or LPS could be suppressed by MK-801 or LY235959. The data demonstrate that prior antagonism of NMDA receptors in the brain, in addition to reducing prostaglandin E2 production in the hypothalamus, suppresses both the glutamate- and LPS-induced fever and increased hypothalamic hydroxyl radicals.
机译：本研究的目的是探讨脑室内给予N-甲基-D-天冬氨酸（NMDA）-受体拮抗剂（MK-801和LY235959）对核心温度和下丘脑2,3-二羟基苯甲酸水平变化的影响脑室内注射谷氨酸（100-400微克，每10微升/兔子）或家兔静脉内注射脂多糖（LPS）（2微克/千克）所诱导的酸（2,3-DHBA）。 2,3-DHBA的测量值用作下丘脑内羟基自由基水平的指标。脑室内注射谷氨酸或静脉内注射LPS均可引起核心温度和下丘脑2,3-DHBA的升高。谷氨酸或LPS注射前1小时，通过注射MK-801或LY235959进行预处理，可明显拮抗谷氨酸或LPS引起的发烧和下丘脑2,3-DHBA水平的升高。 MK-801或LY235959可以抑制谷氨酸或LPS诱导的下丘脑中前列腺素E2的水平升高。数据表明，大脑中NMDA受体的先前拮抗作用，除了减少下丘脑中前列腺素E2的产生外，还抑制了谷氨酸和LPS引起的发烧并增加了下丘脑羟自由基。

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