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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Methamphetamine-induced neurotoxicity in mouse brain is attenuated by ketoprofen, a non-steroidal anti-inflammatory drug.
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Methamphetamine-induced neurotoxicity in mouse brain is attenuated by ketoprofen, a non-steroidal anti-inflammatory drug.

机译:苯丙胺是一种非甾体类抗炎药,可减轻甲基苯丙胺对小鼠大脑的神经毒性。

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摘要

We examined effects of non-steroidal anti-inflammatory drugs (NSAIDs) on methamphetamine (METH)-induced neurotoxicity. Marked reduction of dopamine transporter-positive signals and accumulation of microglial cells in the striatum after METH injections (4 mg/kg x4, i.p. with 2 h-interval) were significantly and dose-dependently attenuated by four injections of ketoprofen (2 or 5 mg/kg x4, s.c.) given 30 min prior to each METH injection, but not by either a low or high dose of aspirin. The present results suggest that the protective effects of ketoprofen against METH-induced neurotoxicity and microgliosis might be based on its inhibitory activity on inflammatory response or on microglia activation, but not on its cyclooxygenase-inhibiting property. This provides a possible new strategy against METH-induced neurotoxicity using commonly used NSAIDs.
机译:我们检查了非甾体抗炎药(NSAIDs)对甲基苯丙胺(METH)诱导的神经毒性的影响。 METH注射(4 mg / kg x4,腹膜内注射2 h间隔)后,多巴胺转运蛋白阳性信号的明显减少和纹状体中小胶质细胞的积累通过注射四次酮洛芬(2或5 mg)显着且剂量依赖性地减弱每次METH注射前30分钟给予/ kg x4,sc),但不给予低剂量或高剂量的阿司匹林。目前的结果表明,酮洛芬对METH诱导的神经毒性和小胶质细胞增生的保护作用可能是基于其对炎症反应的抑制活性或小胶质细胞的活化,而不是基于其对环氧合酶的抑制作用。这提供了使用常用的NSAID对抗METH诱导的神经毒性的可能的新策略。

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