TLR4/NF-κB/NLRP3通路抑制炎症反应作用的研究

Study on the inhibitory effect of TLR4/NF-κB/NLRP3 pathway on inflammatory response

Toll样受体(TLRs)是参与非特异性免疫的一类重要的蛋白质,是表达与固有免疫细胞最重要的模式识别受体之一,可识别来源于微生物的具有保守结构的分子,即病原体相关分子模式(PAMAs),从而激活机体产生免疫应答。核因子κB(NF-κB)在几乎所有类型的细胞和组织中都有表达,在调节对外部刺激的显著多样性的反应中起着关键作用,因此是多个生理和病理过程中的关键因素。而核苷酸结合寡聚化结构域样受体蛋白3(NLRP3),即NLRP3炎性小体通路在脑缺血再灌注和焦亡中具有重要意义,如NLRP3在脑缺血再灌注损伤时在小胶质细胞中被激活,随后在神经元和微血管内皮细胞中表达。由TLRs激活、NF-κB传递、NLRP3启动形成的TLR/NF-κB/NLRP3信号通路在机体各器官炎症反应中起到关键性作用,本文探讨了各类药物通过抑制该通路炎症反应,起到保护身体各大重要器官的作用。

Toll-like receptors(TLRs)are an important class of proteins involved in non-specific immunity,and they are one of the most important pattern recognition receptors expressed by innate immune cells.They can recognize conserved structure molecules from microorganisms,namely pathogen-associated molecular patterns(PAMAs),so as to activate the immune response.Nuclear factor kappa-B(NF-κB),which is expressed in virtually all types of cells and tissues,plays a key role in regulating the remarkable diversity of responses to external stimuli and is therefore a key factor in multiple physiological and pathological processes.NOD-like receptor protein 3(NLRP3),the NLRP3 inflammasome pathway,plays an important role in cerebral ischemia-reperfusion and pyroptosis.For example,NLRP3 is activated in microglia during cerebral ischemia-reperfusion injury and subsequently expressed in neurons and microvascular endothelial cells.The TLR/NF-κB/NLRP3 signaling pathway,which is activated by TLRs,transmitted by NF-κB and activated by NLRP3,plays a key role in the inflammatory response of various organs in the body.This paper discusses the role of various drugs in protecting major organs by inhibiting the inflammatory response of this pathway.