[关键词]
[摘要]
胆红素是体内血红素分解代谢的主要终产物。作为一种内源性抗氧化剂,胆红素可以通过调控氧化应激稳态、核因子E2相关因子2/血红素加氧酶-1(Nrf2/HO-1)信号通路、Toll样受体4/髓分化因子88/核因子-κB(TLR4/Myd88/NF-κB)信号通路、丝裂原活化蛋白激酶(MAPK)信号通路、线粒体功能稳态、生长停滞特异性蛋白6/酪氨酸激酶/细胞因子信号转导抑制因子3(Gas6-Axl-SOCS3)信号轴、过氧化物酶体增殖物激活受体(PPAR)信号通路发挥抗炎作用。梳理了胆红素从分子、细胞器、细胞层面的抗炎作用分子机制,明确其在生理环境下的生物学活性,以期为胆红素的临床应用和药物研发提供参考。
[Key word]
[Abstract]
Bilirubin is the main end-product of heme catabolism in the body. As an endogenous antioxidant, bilirubin can exert anti-inflammatory effects by regulating oxidative stress homeostasis, Nrf2/HO-1 signaling pathway, TLR4/Myd88/NF-κB signaling pathway, MAPK signaling pathway, mitochondrial functional homeostasis, Gas6-Axl-SOCS3 signaling axis, and PPAR signaling pathway. This article summarizes the molecular mechanisms of anti-inflammatory effects of bilirubin from molecular, organelle, and cellular levels, clarifying its biological activity in physiological environments, in order to provide reference for the clinical application and drug development of bilirubin.
[中图分类号]
R965
[基金项目]
天津市科技计划项目(24ZYJDSS00300)