Ligninoformic acid improved DSS-induced chronic colitis in mice by regulating intestinal flora and intestinal barrier

Microb Pathog. 2025 Aug:205:107670. doi: 10.1016/j.micpath.2025.107670. Epub 2025 May 8.

Abstract

Inflammatory Bowel Disease (IBD) is a complex intestinal disorder that typically triggers inflammatory responses, immune dysregulation, and gut microbiota imbalance. Lignoformic acid (LFA) is a lignin-derived compound containing benzene rings and hydroxyl functional groups. It has antioxidant properties and can regulate intestinal pH. This study aimed to investigate the improve effects of LFA on dextran sulfate sodium (DSS)-induced chronic colitis in mice. The results showed that LFA treatment significantly improved body weight and Disease Activity Index (DAI) in mice and alleviated colon damage. In terms of oxidative stress and anti-inflammatory effects, the expression of antioxidant enzymes such as Glutathione Peroxidase (GSH-PX) and Superoxide Dismutase (SOD) was dose-dependently enhanced in DSS-induced mice. LFA reduced the expression of Tumor Necrosis Factor-alpha (TNF-α) by modulating the TLR4/MyD88/NF-κB signaling pathway. Furthermore, LFA dose-dependently increased the abundance of beneficial bacteria, including Akkermansia and Lachnospiraceae, and promoted the production of short-chain fatty acids (SCFAs). These findings suggest that LFA could serve as a therapeutic agent for colitis by enhancing intestinal barrier integrity, regulating inflammation, and restoring gut microbiota balance.

Keywords: Gut microbiota; Inflammatory bowel disease; Intestinal barrier; Lignoformic acid; Oxidative stress.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Antioxidants / pharmacology
  • Chronic Disease
  • Colitis* / chemically induced
  • Colitis* / drug therapy
  • Colitis* / microbiology
  • Colitis* / pathology
  • Colon / drug effects
  • Colon / pathology
  • Dextran Sulfate / adverse effects
  • Disease Models, Animal
  • Fatty Acids, Volatile / metabolism
  • Gastrointestinal Microbiome* / drug effects
  • Glutathione Peroxidase / metabolism
  • Intestinal Mucosa* / drug effects
  • Lignin* / analogs & derivatives
  • Lignin* / pharmacology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Myeloid Differentiation Factor 88 / metabolism
  • NF-kappa B / metabolism
  • Oxidative Stress / drug effects
  • Signal Transduction / drug effects
  • Superoxide Dismutase / metabolism
  • Toll-Like Receptor 4 / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Dextran Sulfate
  • Tumor Necrosis Factor-alpha
  • Toll-Like Receptor 4
  • Lignin
  • NF-kappa B
  • Myeloid Differentiation Factor 88
  • Tlr4 protein, mouse
  • Fatty Acids, Volatile
  • Superoxide Dismutase
  • Antioxidants
  • Anti-Inflammatory Agents
  • Glutathione Peroxidase