Neohesperidin Attenuates DSS-Induced Ulcerative Colitis by Inhibiting Inflammation, Reducing Intestinal Barrier Damage, and Modulating Intestinal Flora Composition.
Tianyuan JuZheyu SongDi QinJi ChengTong LiGuiqiu HuShoupeng FuPublished in: Journal of agricultural and food chemistry (2024)
Flavonoid natural products are emerging as a promising approach for treating Ulcerative Colitis (UC) due to their natural origin and minimal toxicity. This study investigates the effects of Neohesperidin (NEO), a natural flavonoid, on Dextran Sodium Sulfate (DSS)-induced UC in mice, focusing on the underlying molecular mechanisms. Early intervention with NEO (25 and 50 mg/kg) mitigated colon shortening, restored damaged barrier proteins, and significantly reduced the inflammatory cytokine levels. Moreover, NEO inhibited the MAPK/NF-κB signaling pathway and enhanced the levels of intestinal barrier proteins (Claudin-3 and ZO-1). Additionally, NEO increased beneficial intestinal probiotics ( S24-7 and Lactobacillaceae ) while reducing harmful bacteria ( Erysipelotrichi , Enterobacteriaceae ). Fecal microbial transplantation (FMT) results demonstrated that NEO (50 mg/kg) markedly improved UC symptoms. In conclusion, early NEO intervention may alleviate DSS-induced UC by inhibiting inflammatory responses, preserving intestinal barrier integrity and modulating gut microbiota.
Keyphrases
- signaling pathway
- oxidative stress
- diabetic rats
- ulcerative colitis
- pi k akt
- high glucose
- randomized controlled trial
- drug induced
- induced apoptosis
- type diabetes
- stem cells
- pseudomonas aeruginosa
- immune response
- microbial community
- physical activity
- inflammatory response
- escherichia coli
- lps induced
- insulin resistance
- cell proliferation
- nuclear factor