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Xinyan Qu,Yingying Song,Qingjun Li,Qi Xu,Yanru Li,Huimin Zhang,Xuemei Cheng,Charles R. Mackay,Quanbo Wang,Wei Liu 대한약학회 2024 Archives of Pharmacal Research Vol.47 No.3
Microbiota-derived catabolism of nutrients is closely related to ulcerative colitis (UC). The level of indole-3-acetic acid(IAA), a microbiota-dependent metabolite of tryptophan, was decreased signifi cantly in the feces of UC patients. Thus supplementationwith IAA could be a potential therapeutic method for ameliorating colitis. In this work, the protective eff ect ofsupplementation with IAA on dextran sulfate sodium (DSS)-induced colitis was evaluated, and the underlying mechanismwas elucidated. The results indicated that the administration of IAA signifi cantly relieved DSS-induced weight loss, reducedthe disease activity index (DAI), restored colon length, alleviated intestinal injury, and improved the intestinal tight junctionbarrier. Furthermore, IAA inhibited intestinal infl ammation by reducing the expression of proinfl ammatory cytokines andpromoting the production of IL-10 and TGF-β1. In addition, the ERK signaling pathway is an important mediator of variousphysiological processes including infl ammatory responses and is closely associated with the expression of IL-10. Notably,IAA treatment induced the activation of extracellular signal-regulated kinase (ERK), which is involved in the progressionof colitis, while the ERK inhibitor U0126 attenuated the benefi cial eff ects of IAA. In summary, IAA could attenuate theclinical symptoms of colitis, and the ERK signaling pathway was involved in the underlying mechanism. Supplementationwith IAA could be a potential option for preventing or ameliorating UC.
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