首页> 外文期刊>International immunopharmacology >Molecular mechanisms of anti-inflammatory effect of chrysophanol, an active component of AST2017-01 on atopic dermatitis in vitro models
【24h】

Molecular mechanisms of anti-inflammatory effect of chrysophanol, an active component of AST2017-01 on atopic dermatitis in vitro models

机译:汉霉素抗炎作用的分子机制,体外模型AST2017-01的活性成分

获取原文
获取原文并翻译 | 示例
           

摘要

AST2017-01 mainly consists of Rumex crispus and -Cordyceps militaris and has been widely consumed as an herbal medicine or functional food in Korea. Here we investigated the influences of AST2017-01 and its active component, chrysophanol on human mast cell (HMC-1 cell) and human keratinocyte (HaCaT cell)-mediated inflammatory reactions. Pretreatment with AST2017-01 or chrysophanol suppressed intracellular calcium levels and histamine release in phorbol 12-myristate 13-acetate and calcium ionophore A23187 (PMACI)-treated HMC-1 cells. Levels of phosphorylated-mitogen-activated protein kinase increased by PMACI stimulation were reduced by AST2017-01 or chrysophanol pretreatment. Protein levels of I kappa B kinase beta and receptor-interacting protein 2 in PMACI-treated HMC-1 cells were decreased by AST2017-01 or chrysophanol pretreatment. Pretreatment with AST2017-01 or chrysophanol significantly blocked PMACI-induced activation of caspase-1 and nuclear factor-kappa B. In addition, pretreatment with AST2017-01 or chrysophanol significantly decreased the PMACI-induced levels of interleukin (IL)-1 beta, IL-6, tumor necrosis factor-a, and thymic stromal lymphopoietin (TSLP) on HMC-1 cells. In activated HaCaT cells, pretreatment with AST2017-01 or chrysophanol significantly reduced production of TSLP and activation of caspase-1. In conclusion, these findings indicate that chrysophanol is an active component of AST2017-01 and AST2017-01 acts as a novel potent anti-inflammatory herbal medicine or functional food.
机译:AST2017-01主要包括RUMEX CRISPUS和-CORDYCEPS MILITARIS,并且已被广泛消耗作为韩国的草药或功能性食品。在这里,我们研究了AST2017-01及其活性成分的影响,Chrysophanol对人肥大细胞(HMC-1细胞)和人角蛋白细胞(HaCAT细胞)介导的炎症反应。用AST2017-01或氯氰酸抑制的预处理抑制了富宝栓12- myristerate 13-乙酸盐和钙离子载体A23187(PMACI)-Treated HMC-1细胞中的细胞内钙水平和组胺释放。 AST2017-01或Chrysophanol预处理减少了通过PMACI刺激增加的磷酸化丝裂型蛋白激活蛋白激酶的水平。通过AST2017-01或Chrysophanol预处理降低了PMACI处理的HMC-1细胞中的I Kappa B激酶β和受体相互作用蛋白2的蛋白质水平。使用AST2017-01或甲醇的预处理显着堵塞了PMACI诱导的Caspase-1和核因子-Kappa B的激活。此外,与AST2017-01或甲醇的预处理显着降低了白细胞介素(IL)-1β的PMACI诱导的水平, IL-6,肿瘤坏死因子-A和胸腺基质淋巴胞苷(TSLP)对HMC-1细胞。在活化的HaCAT细胞中,用AST2017-01或甲醇的预处理显着降低了TSLP的产生和Caspase-1的活化。总之,这些发现表明,甲醇是AST2017-01和AST2017-01的活性组分,作为新型有效的抗炎药物或功能性食品。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号