吲哚乙酸的抗炎特性研究  

Study on anti-inflammatory properties of indole-3-acetic acid

作　　者：蔡毓玮 管彤 张泽 曹琬晴 陆瑶 郑魏 李森[1,2] CAI Yuwei;GUAN Tong;ZHANG Ze;CAO Wanqing;LU Yao;ZHENG Wei;LI Sen(School of Health Science and Engineering,University of Shanghai for Science and Technology,Shanghai 200093,China;National Grain Industry(Urban Grain and Oil Security)Technology Innovation Center,Shanghai 200093,China)

机构地区：[1]上海理工大学健康科学与工程学院,上海200093 [2]国家粮食产业(城市粮油保障)技术创新中心,上海200093

出　　处：《食品与发酵工业》2025年第4期98-103,共6页Food and Fermentation Industries

基　　金：国家自然科学基金项目(31901609)。

摘　　要：吲哚乙酸(indole-3-acetic acid,IAA)是色氨酸的代谢产物。为了探究IAA对神经炎症的调控作用,该研究建立了脂多糖(lipopolysaccharide,LPS)诱导的SH-SY5Y神经细胞炎症模型。首先通过细胞活性检测确定了LPS的诱导剂量,并检测了IAA对SH-SY5Y细胞活性的影响,然后利用蛋白免疫印迹测定了细胞中的炎症因子的表达情况,并对肿瘤坏死因子受体超家族成员25(tumor necrosis factor receptor superfamily 25,Tnfrsf25)/IκB激酶(inhibitor of kappa B kinase,IKK)/核因子κB(nuclear factor kappa-B,NF-κB)信号通路相关蛋白的表达水平进行检测。结果表明,低剂量的IAA不会影响SH-SY5Y细胞的存活率,超过200μg/mL的IAA处理才会对细胞的存活率造成显著影响;IAA处理可显著抑制LPS引起的TNF-α和IL-1β的蛋白水平升高;此外,IAA可显著下调Tnfrsf25的蛋白水平,抑制IKK、IκB-α、NF-κB的磷酸化,表明IAA通过调控Tnfrsf25/IKK/NF-κB信号通路发挥抑制神经炎症的作用。该项目为阐明色氨酸代谢对脑部的保护作用提供了理论依据。Indole-3-acetic acid(IAA)is a metabolite of tryptophan.To investigate the regulatory effect of IAA on neuroinflammation,this study established an SH-SY5Y neuroinflammation cell model induced by lipopolysaccharide(LPS).Firstly,the induction dosage of LPS was determined through cell viability assays,and the impact of IAA on the viability of SH-SY5Y cells was evaluated.Then,Western bolt was used to determine the expression of inflammatory factors and the expression levels of proteins related to the tumor necrosis factor receptor superfamily 25(Tnfrsf25)/inhibitor of kappa B kinase(IKK)/nuclear factor kappa-B(NF-κB)signaling pathway in the cells.Results demonstrated that low dosages of IAA had no impact on the survival rate of SH-SY5Y cells;however,notable effects on cell viability were observed when the concentration of IAA exceeded 200μg/mL.IAA treatment significantly inhibited the elevation of tumor necrosis factor-α(TNF-α)and interleukin-1β(IL-1β)induced by LPS.Additionally,IAA markedly downregulated the protein levels of Tnfrsf25 and suppressed the phosphorylation of IKK,IκB-α,and NF-κB,indicating that IAA might exert inhibitory effect on neuroinflammation by modulating the Tnfrsf25/IKK/NF-κB signaling pathway.This study provides theoretical evidence for the neuroprotective role of tryptophan metabolism.

关 键 词：吲哚乙酸 SH-SY5Y细胞 神经炎症 NF-ΚB信号通路 

分 类 号：R965[医药卫生—药理学]