Safflower Polysaccharides Alleviate TNBS-Induced Colitis by Modulating Gut Immunity.

Area of Science:

• Immunology
• Gastroenterology
• Pharmacology

Background:

• Colitis is a chronic inflammatory condition of the colon with limited therapeutic options.
• Understanding the immunological mechanisms underlying colitis is crucial for developing effective treatments.
• Safflower polysaccharides (SPSs) have shown potential in traditional medicine, but their immunomodulatory effects in colitis require detailed investigation.

Purpose of the Study:

• To elucidate the immunological mechanisms by which Safflower polysaccharides (SPSs) regulate colitis.
• To evaluate the therapeutic effects of SPSs on a rat model of colitis and in vitro cellular models.
• To identify key molecular pathways and cellular interactions involved in SPSs' anti-colitis effects.

Main Methods:

• Induction of colitis in rats using trinitrobenzene sulfonic acid (TNBS).
• In vitro studies using TNF-α-stimulated Caco-2 cells, LPS-induced THP-1 cells, and co-culture models.
• Investigation of CHI3L1's role using siRNA and recombinant CHI3L1 (r-CHI3L1).
• Analysis of STAT3/NF-κB signaling pathways.

Main Results:

• SPSs significantly ameliorated clinical symptoms and colonic pathological damage in TNBS-induced colitis rats.
• SPSs reduced pro-inflammatory factors, inhibited macrophage M1 polarization, and restored colonic immunity in vivo.
• In vitro, SPSs alleviated epithelial cell inflammation, inhibited macrophage M1 polarization, and regulated epithelial-immune cell interactions.
• CHI3L1 was identified as a mediator of epithelial-immune cell interactions, crucial for SPSs' immunomodulatory effects.
• STAT3/NF-κB signaling pathways were implicated in the therapeutic mechanisms of SPSs.

Conclusions:

• Safflower polysaccharides (SPSs) demonstrate significant therapeutic efficacy in colitis models.
• SPSs exert their effects through immunomodulation, including the inhibition of macrophage M1 polarization and regulation of epithelial-immune cell crosstalk via CHI3L1.
• The findings highlight SPSs as a promising agent for colitis treatment, acting through STAT3/NF-κB signaling and CHI3L1-mediated mechanisms.