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首页> 外文期刊>Journal of pharmacological sciences. >Aspirin may exert its antipyresis by inhibiting the N-methyl-D-aspartate receptor-dependent hydroxyl radical pathways in the hypothalamus.
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Aspirin may exert its antipyresis by inhibiting the N-methyl-D-aspartate receptor-dependent hydroxyl radical pathways in the hypothalamus.

机译：阿司匹林可能通过抑制下丘脑中的N-甲基-D-天冬氨酸受体依赖性羟基自由基途径发挥其解热作用。

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摘要

Recent findings have suggested that the N-methyl-D-aspartate (NMDA) receptor-dependent hydroxyl radical pathway in the hypothalamus of rabbit brain may mediate the fever induced by lipopolysaccharide (LPS). The aim of this study was to investigate whether aspirin exerts its antipyresis by suppressing hypothalamic glutamate and hydroxyl radicals in rabbits. The microdialysis probes were stereotaxically and chronically implanted into the preoptic anterior hypothalamus of rabbit brain for determination of both glutamate and hydroxyl radicals in situ. It was found that intravenous (i.v.) injection of LPS, in addition to inducing fever, caused increased levels of both glutamate and hydroxyl radicals in the hypothalamus. Pretreatment with aspirin (10 - 60 mg/kg, i.v.) one hour before an i.v. dose of LPS significantly reduced the febrile response and attenuated the LPS-induced increased levels of both glutamate and hydroxyl radicals in the hypothalamus. The increased levels of prostaglandin E(2) (PGE(2)) in the hypothalamus induced by LPS could be suppressed by aspirin pretreatment. The data indicate that systemic administration of aspirin, in addition to suppressing PGE(2) production, may exert its antipyresis by inhibiting the NMDA receptor-dependent hydroxyl radical pathways in the hypothalamus during LPS fever.
机译：最近的发现表明，兔脑下丘脑中的N-甲基-D-天冬氨酸（NMDA）受体依赖性羟基自由基途径可能介导脂多糖（LPS）诱导的发烧。这项研究的目的是研究阿司匹林是否通过抑制家兔下丘脑谷氨酸和羟自由基发挥其解热作用。将微透析探针立体定位并长期植入兔脑的视前前下丘脑中，以原位测定谷氨酸和羟自由基。已经发现，静脉注射LPS除了引起发烧外，还引起下丘脑中谷氨酸和羟自由基水平的增加。静脉注射前一小时用阿司匹林（10-60 mg / kg，静脉注射）进行预处理。 LPS剂量显着降低了发热反应，并减弱了LPS诱导的下丘脑中谷氨酸和羟自由基水平的升高。阿司匹林预处理可抑制LPS诱导的下丘脑中前列腺素E（2）（PGE（2））的水平升高。数据表明，阿司匹林的全身性给药，除了抑制PGE（2）的产生外，还可能通过抑制LPS发热下丘脑中NMDA受体依赖性羟基自由基途径发挥其退热作用。

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