Sotetsuflavone ameliorates Crohn's disease-like colitis by inhibiting M1 macrophage-induced intestinal barrier damage via JNK and MAPK signalling

Eur J Pharmacol. 2023 Feb 5:940:175464. doi: 10.1016/j.ejphar.2022.175464. Epub 2022 Dec 22.

Abstract

Objectives: Intestinal inflammation and intestinal barrier dysfunction are two important pathological changes in Crohn's disease (CD). Sotetsuflavone (SF) is a natural monomeric herbal compound with anti-inflammatory and cytoprotective effects that is mostly nontoxic. The effect of SF on CD-like spontaneous colitis was investigated in this study.

Methods: Il-10-/- mice were used as a CD model and were administered different doses of SF. Lipopolysaccharide (LPS) plus IFN-γ-induced macrophages (RAW264.7) and a coculture system (RAW264.7 and organoids) were used in vitro. The protective effects of SF against CD-like colitis and macrophage differentiation and the mechanisms were evaluated.

Results: SF treatment markedly improved spontaneous colitis in the CD model, as shown by the following evidence: reductions in the DAI, macroscopic scores (3.63 ± 1.30), colonic tissue inflammatory scores (2 ± 0.76) and proinflammatory factor levels and the attenuation of colon shortening (8 ± 0.93 cm) and weight loss (1.75 ± 1.83 g). Decreased intestinal permeability and intestinal bacterial translocation rates provided evidence of the protective effect of SF on intestinal barrier function. We also found that SF suppressed M1 macrophage-induced inflammatory responses. In the coculture system of mouse colonic organoids and RAW264.7 cells, SF significantly ameliorated M1 macrophage-induced intestinal epithelial damage. In addition, SF inhibited JNK and MAPK (p38) signalling in both Il-10-/- mice and LPS plus IFN-γ-induced macrophages (RAW264.7).

Conclusions: The protective effects of SF against CD-like colitis may be achieved partially by inhibiting M1 macrophage-induced intestinal barrier damage via JNK and p38 signalling. SF may have therapeutic potential for treating CD, especially considering its safety.

Keywords: Crohn's disease; Intestinal barrier function; MAPK; Macrophages; Sotetsuflavone.

MeSH terms

  • Animals
  • Colitis* / chemically induced
  • Colitis* / drug therapy
  • Colitis* / pathology
  • Colon / pathology
  • Crohn Disease* / drug therapy
  • Cytokines / pharmacology
  • Dextran Sulfate / adverse effects
  • Interleukin-10
  • Lipopolysaccharides / adverse effects
  • MAP Kinase Signaling System*
  • Macrophages
  • Mice
  • Mice, Inbred C57BL

Substances

  • Cytokines
  • Dextran Sulfate
  • Interleukin-10
  • Lipopolysaccharides
  • sotetsuflavone