论文部分内容阅读
为探索姜辣素拮抗掌叶半夏毒针晶刺激性毒性的机制,该研究采用掌叶半夏毒针晶诱导的小鼠腹腔炎症模型,观察姜辣素对小鼠腹腔炎症渗出液中炎症介质PGE2的影响;采用大鼠腹腔巨噬细胞体外培养模型,以上清液中TNF-α和IL-1β为指标,研究姜辣素拮抗掌叶半夏毒针晶的致炎作用;采用扫描电镜法观察姜辣素拮抗掌叶半夏毒针晶刺激后巨噬细胞表面形态的改变;采用巨噬细胞-中性粒细胞共培养模型,考察姜辣素拮抗掌叶半夏毒针晶对中性粒细胞迁移的影响。结果显示,姜辣素可以显著抑制掌叶半夏毒针晶所致的小鼠腹腔渗出液中PGE2的生成;姜辣素可以显著抑制掌叶半夏毒针晶诱导巨噬细胞释放炎症因子,并具有一定的量效关系;扫描电镜显示,姜辣素可以显著抑制巨噬细胞吞噬掌叶半夏毒针晶及细胞膜破损,并能显著抑制掌叶半夏毒针晶诱导的中性粒细胞迁移。姜辣素拮抗掌叶半夏毒针晶刺激性毒性的机制可能是抑制了包括巨噬细胞激活、炎症因子释放、中性粒细胞迁移聚集的致炎毒性。
In order to explore the mechanism of Gingerol antagonizing the irritant toxicity of Radix Platycodonis Indicae, the model of mouse abdominal cavity inflammation induced by Radix Platycodonis was prepared. The effect of Gingerol on the expression of PGE2 The rat model of peritoneal macrophages in vitro was established. The TNF-α and IL-1β in the supernatant were used as indexes to study the anti-inflammatory effects of gingerol on the needle-punctate needle crystalloid. Antagonize the change of surface morphology of macrophages induced by acupuncture at Arnebia euchroma pallidis. Use macrophage-neutrophil co-culture model to investigate the effect of gingerol on the migration of neutrophils by antagonizing the needles. The results showed that gingerol could significantly inhibit the generation of PGE2 in mouse peritoneal exudate induced by Armpitaxia tabacum; Gingerol could significantly inhibit the release of inflammatory cytokines by macrophages from Gynura divaricatum, The results of scanning electron microscopy showed that Gingerol could significantly inhibit macrophage phagocytosis of P. tuberosum and the damage of cell membrane, and significantly inhibit the neutrophil migration induced by P. armeniacum. The mechanism by which Gingerol antagonizes the acute toxic effects of Gynura divaricatum may inhibit the inflammatory cytotoxicity including macrophage activation, release of inflammatory cytokines and neutrophil migration and aggregation.