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从红海藻角叉菜(Hypnea cervicornis J. Agardh)中分离出的凝集素可减轻炎症性痛觉过敏:涉及一氧化氮。

Agglutinin isolated from the red marine alga Hypnea cervicornis J. Agardh reduces inflammatory hypernociception: involvement of nitric oxide.

机构信息

Department of Biochemistry and Molecular Biology, Federal University of Ceara, 60451-970, Fortaleza-CE, Brazil.

出版信息

Pharmacol Biochem Behav. 2010 Oct;96(4):371-7. doi: 10.1016/j.pbb.2010.06.008. Epub 2010 Jun 30.

Abstract

Hypnea cervicornis agglutinin (HCA), a lectin isolated from the red marine alga has been previously shown to have an antinociceptive effect. In the present study in rats, mechanisms of action of HCA were addressed regarding mechanical hypernociception induced by carrageenan, ovalbumin (as antigen), and also by prostaglandin E(2) in rats. The lectin administered intravenously inhibited carrageenan- and antigen-induced hypernociception at 1, 3, 5 and 7h. This inhibitory effect was completely prevented when lectin was combined with mucin, demonstrating the role of carbohydrate-binding sites. The inhibition of inflammatory hypernociception by HCA was associated with the prevention of neutrophil recruitment to the plantar tissue of rats but was not associated with the inhibition of the release of pro-hypernociceptive cytokines (TNF-alpha, IL-1 beta and CINC-1). HCA also blocked mechanical hypernociception induced by PGE(2), which was prevented by the administration of nitric oxide synthase inhibitors. These results were corroborated by the increased circulating levels of NO metabolites following HCA treatment. These findings suggest that the anti-hypernociceptive effects of HCA are not associated with the inhibition of pro-inflammatory cytokine production. However, these effects seem to involve the inhibition of neutrophil migration and also the increase in NO production.

摘要

齿缘墨角藻凝集素(HCA)是从红海藻中分离出的一种凝集素,先前已显示其具有镇痛作用。在本研究中,我们研究了 HCA 对角叉菜胶、卵清蛋白(作为抗原)以及前列腺素 E2 诱导的机械性痛觉过敏的作用机制。静脉内给予凝集素可抑制角叉菜胶和抗原诱导的痛觉过敏,在 1、3、5 和 7 小时时抑制作用最强。当凝集素与粘蛋白联合使用时,这种抑制作用完全被阻止,表明糖结合位点的作用。HCA 抑制炎症性痛觉过敏与预防中性粒细胞募集到大鼠足底组织有关,但与抑制促痛觉过敏细胞因子(TNF-α、IL-1β和 CINC-1)的释放无关。HCA 还可阻断 PGE2 诱导的机械性痛觉过敏,一氧化氮合酶抑制剂可阻止这种作用。这些结果得到了 HCA 治疗后循环中 NO 代谢物水平升高的证实。这些发现表明,HCA 的抗痛觉过敏作用与抑制促炎细胞因子的产生无关。然而,这些作用似乎涉及抑制中性粒细胞迁移和增加 NO 生成。

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