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姜烯酮的镇痛作用:涉及 L-精氨酸-一氧化氮-cGMP-PKC-K+ATP 通道途径。

Zerumbone-induced antinociception: involvement of the L-arginine-nitric oxide-cGMP -PKC-K+ ATP channel pathways.

机构信息

Department of Biomedical Science, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, Selangor, Malaysia.

出版信息

Basic Clin Pharmacol Toxicol. 2011 Mar;108(3):155-62. doi: 10.1111/j.1742-7843.2010.00635.x. Epub 2010 Oct 18.

DOI:10.1111/j.1742-7843.2010.00635.x
PMID:20955360
Abstract

This study investigated the antinociceptive effects of zerumbone in chemical behavioural models of nociception in mice. Zerumbone given through intraperitoneal route (i.p.) produced dose-related antinociception when assessed on acetic acid-induced abdominal writhing test in mice. In addition, the i.p. administration of zerumbone exhibited significant inhibition of the neurogenic pain induced by intraplantar (i.pl.) injection of capsaicin and bradykinin. Likewise, zerumbone given by i.p. route reduced the nociception produced by i.pl. injection of glutamate and phorbol myristate acetate (PMA). The antinociception caused by zerumbone in the acetic acid test was significantly attenuated by i.p. pre-treatment of mice with l-arginine (nitric oxide precursor) and glibenclamide (ATP-sensitive K(+) channel inhibitor). However, the antinociception of zerumbone was enhanced by methylene blue (non-specific gyanylyl cyclase inhibitor). Together, these results indicate that zerumbone produces pronounced antinociception against chemical models of nociception in mice. It also strongly suggests that the l-arginine-nitric oxide-cGMP-PKC-K(+) ATP channel pathways, the TRPV1 and kinin B2 receptors play an important role in the zerumbone-induced antinociception.

摘要

本研究探讨了姜烯酮在小鼠伤害性感受化学行为模型中的镇痛作用。腹腔给予姜烯酮可剂量依赖性地减轻醋酸诱导的小鼠扭体反应。此外,腹腔给予姜烯酮可显著抑制足底(i.pl.)注射辣椒素和缓激肽引起的神经源性疼痛。同样,腹腔给予姜烯酮可减轻 i.pl. 注射谷氨酸和佛波醇十四酸乙酯(PMA)引起的疼痛。腹腔给予姜烯酮可显著减弱 l-精氨酸(一氧化氮前体)和格列本脲(ATP 敏感性 K+通道抑制剂)预处理对醋酸试验中姜烯酮引起的镇痛作用。然而,姜烯酮的镇痛作用可被亚甲蓝(非特异性鸟苷酸环化酶抑制剂)增强。综上所述,这些结果表明姜烯酮对小鼠伤害性感受化学模型具有显著的镇痛作用。此外,研究结果还表明,l-精氨酸-一氧化氮-cGMP-PKC-K+ATP 通道途径、TRPV1 和激肽 B2 受体在姜烯酮诱导的镇痛作用中发挥着重要作用。

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