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黄酮类化合物在炎症反应中对炎症小体激活的调控作用。

Regulatory Roles of Flavonoids on Inflammasome Activation during Inflammatory Responses.

机构信息

Department of Pharmaceutical Engineering, Cheongju University, Cheongju, 28503, Korea.

出版信息

Mol Nutr Food Res. 2018 Jul;62(13):e1800147. doi: 10.1002/mnfr.201800147. Epub 2018 Jun 19.

DOI:10.1002/mnfr.201800147
PMID:29774640
Abstract

Inflammation is an innate immune response to noxious stimuli to protect the body from pathogens. Inflammatory responses consist of two main steps: priming and triggering. In priming, inflammatory cells increase expressions of inflammatory molecules, while in triggering, inflammasomes are activated, resulting in cell death and pro-inflammatory cytokine secretion. Inflammasomes are protein complexes comprising intracellular pattern recognition receptors (PRRs) (e.g., nucleotide-binding oligomerization domain-like receptors (NLRs), absent in melanoma 2 (AIM2), and caspases-4/5/11) and pro-caspase-1 with or without a bipartite adaptor molecule ASC. Inflammasome activation induces pyroptosis, inflammatory cell death, and stimulates caspase-1-mediated secretion of interleukin (IL)-1b and IL-18. Flavonoids are secondary metabolites found in various plants and are considered as critical ingredients promoting health and ameliorating various disease symptoms. Anti-inflammatory activity of flavonoids and underlying mechanisms have been widely studied. This review introduces current knowledge on different types of inflammasomes and their activation during inflammatory responses and discusses recent studies regarding anti-inflammatory roles of flavonoids as suppressors of inflammasomes in inflammatory conditions. Understanding the regulatory effects of flavonoids on inflammasome activation will increase our knowledge of flavonoid-mediated anti-inflammatory activity and provide new insights into the development of flavonoid preparations to prevent and treat human inflammatory diseases.

摘要

炎症是一种对有害刺激的先天免疫反应,旨在保护身体免受病原体侵害。炎症反应由两个主要步骤组成:启动和触发。在启动过程中,炎症细胞增加炎症分子的表达,而在触发过程中,炎性小体被激活,导致细胞死亡和促炎细胞因子的分泌。炎性小体是由细胞内模式识别受体(PRRs)(例如,核苷酸结合寡聚化结构域样受体(NLRs)、黑色素瘤 2 缺失(AIM2)和胱天蛋白酶-4/5/11)和前胱天蛋白酶-1 组成的蛋白复合物,有或没有双功能衔接子分子 ASC。炎性小体的激活诱导细胞焦亡、炎症细胞死亡,并刺激胱天蛋白酶-1 介导的白细胞介素(IL)-1b 和 IL-18 的分泌。类黄酮是存在于各种植物中的次生代谢产物,被认为是促进健康和改善各种疾病症状的关键成分。类黄酮的抗炎活性及其潜在机制已得到广泛研究。本综述介绍了不同类型的炎性小体及其在炎症反应中的激活的最新知识,并讨论了最近关于类黄酮作为炎性小体抑制剂在炎症条件下发挥抗炎作用的研究。了解类黄酮对炎性小体激活的调节作用将增加我们对类黄酮介导的抗炎活性的认识,并为开发预防和治疗人类炎症性疾病的类黄酮制剂提供新的见解。

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