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[姜辣素对半夏毒性针晶炎症效应的拮抗机制]

[Antagonism mechanism of gingerols against inflammatory effect of toxic raphides from Pinella pedatisecta].

作者信息

Jin Yang-Ping, Wu Hao, Yu Hong-Li, Pan Yao-Zong, Chen Ye-Qing, Wang Kui-Long, Zhang Cheng-Chao, Wang Wei

机构信息

College of Pharmacology, Nanjing University of Traditional Chinese Medicine, Nanjing 210046, China.

Jiangsu Key Laboratory of Traditional Chinese Medicine Processing, Nanjing 210046, China.

出版信息

Zhongguo Zhong Yao Za Zhi. 2016 Mar;41(6):1087-1092. doi: 10.4268/cjcmm20160619.

Abstract

This study was to investigate the mechanism of gingerols antagonizing the inflammatory effect of toxic raphides from Pinella pedatisecta. Mice peritonitis models induced by toxic raphides from P. pedatisecta were applied to observe the effect of gingerols on inflammatory mediators PGE2 in the exudates of abdominal inflammation in mice; rats peritoneal macrophage in vitro culture models were adopted to study the anti-inflammatory effects of gingerol against toxic raphides, with TNF-α and IL-1β in supernatant as indexes. Scanning electron microscopy was used to observe the changes in surface morphology of macrophages treated by raphides and gingerols. Macrophages-neutrophils co-cultured models were used to study the antagonism of gingerols against the effect of toxic raphides' stimulation on neutrophils migration. Results showed that gingerols could significantly inhibit the production of PGE2 in the exudates of abdominal inflammation induced by toxic raphides from P. pedatisecta in mice. Gingerols could significantly inhibit the toxic raphides from P. pedatisecta to induce the release of inflammatory factors, with certain dose dependence. Scanning electron microscopy showed that gingerols could significantly inhibit phagocytosis of macrophages, cytomembrane injury, and neutrophils migration induced by toxic raphides from P. pedatisecta. The results showed that the antagonism mechanism of gingerols against the toxic raphides from P. pedatisecta may be associated with inhibiting the pro-inflammatory toxicity including macrophage activation, inflammatory factors release, and neutrophils migration.

摘要

本研究旨在探讨姜辣素拮抗半夏毒性针晶炎症效应的机制。采用半夏毒性针晶诱导的小鼠腹膜炎模型,观察姜辣素对小鼠腹部炎症渗出液中炎症介质PGE2的影响;采用大鼠腹膜巨噬细胞体外培养模型,以上清液中TNF-α和IL-1β为指标,研究姜辣素对半夏毒性针晶的抗炎作用。利用扫描电子显微镜观察针晶和姜辣素处理后巨噬细胞表面形态的变化。采用巨噬细胞-中性粒细胞共培养模型,研究姜辣素对半夏毒性针晶刺激中性粒细胞迁移作用的拮抗作用。结果表明,姜辣素可显著抑制半夏毒性针晶诱导的小鼠腹部炎症渗出液中PGE2的产生。姜辣素可显著抑制半夏毒性针晶诱导炎症因子的释放,具有一定的剂量依赖性。扫描电子显微镜显示,姜辣素可显著抑制半夏毒性针晶诱导的巨噬细胞吞噬、细胞膜损伤及中性粒细胞迁移。结果表明姜辣素拮抗半夏毒性针晶的作用机制可能与抑制包括巨噬细胞激活、炎症因子释放及中性粒细胞迁移在内的促炎毒性有关。

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