Protective Effects of Aucubin in DSS-Induced Colitis: Modulation of Inflammatory Pathways, Intestinal Barrier Integrity, and Gut Microbiota

TL;DR

Aucubin, a compound from Eucommia leaf, shows protective effects in colitis by reducing inflammation, improving gut health, and balancing gut bacteria.

Contribution

This study is the first to demonstrate aucubin's efficacy in alleviating colitis through multiple mechanisms including microbiota modulation.

Findings

Aucubin reduced inflammation and improved colon health in DSS-induced colitis in mice.

Aucubin modulated gut microbiota by increasing beneficial bacteria and decreasing harmful ones.

Aucubin enhanced intestinal barrier function and reduced inflammatory gene expression in both animal and cell experiments.

Abstract

As an active ingredient in Eucommia leaf, aucubin (AU) is natural and safe, and studies have shown that aucubin (AU) demonstrates great potential in its anti-inflammatory, antioxidant, neuroprotective, and anti-osteoporotic properties. However, AU has been less studied in colitis. In this experiment, we used DSS-induced mice to establish a colitis model to investigate the ability of AU to alleviate colitis. The results show that, in animal experiments, AU increased body weight, reduced disease activity index (DAI) scores and organ indices, restored colon morphology, and increased superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and catalase (CAT) levels in mouse serum and colon. It also reduced malondialdehyde (MDA) levels, decreased the relative mRNA expression levels of inflammatory factors IL-1β, TNF-α, IL-18, MyD88, and NF-κB, and increased the relative mRNA expression levels of intestinal barrier-related genes OCLN, CLDN1, CLDN2, ZO-2, and MUC1. AU also upregulated the abundance of bacterial groups such as Bacteroidota, Firmicutes, and Verrucomicrobiota, and downregulated the abundance of bacterial groups such as Proteobacteria and Deferribacterota, thereby regulating the intestinal microbiota. In cell experiments, AU increased the relative mRNA expression levels of intestinal barrier-related genes MUC2, ZO-1, OCLN, and CLDN1, reduced the relative expression levels of inflammatory factors IL-1β and TNF-α, and increased the relative expression level of the anti-inflammatory factor IL-10. Additionally, AU significantly reduced the relative expression levels of IL-1β, IL-1R, MyD88, TAK1, IKKα, and RelA. This study provides a theoretical and technical basis for the large-scale preparation of aucubin and the alleviation of inflammatory bowel disease.

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