Curcumin Alleviated Dextran Sulfate Sodium-Induced Colitis by Regulating M1/M2 Macrophage Polarization and TLRs...

Area of Science:

• Immunology
• Pharmacology
• Gastroenterology

Background:

• Ulcerative colitis (UC) is a chronic inflammatory bowel disease.
• Curcumin demonstrates therapeutic potential in experimental colitis and human UC.
• The precise mechanism of curcumin's action, particularly regarding macrophage polarization, requires further elucidation.

Purpose of the Study:

• To investigate the therapeutic effects of curcumin in a mouse model of dextran sulfate sodium (DSS)-induced colitis.
• To explore the role of curcumin in regulating M1/M2 macrophage polarization within the colonic tissue.
• To examine the impact of curcumin on the Toll-like receptor (TLR) signaling pathway in colitis.

Main Methods:

• Experimental colitis was induced in mice using DSS.
• Mice were treated with curcumin (10 mg/kg/day) or 5-aminosalicylic acid (5-ASA) (300 mg/kg/day) for 14 days.
• Macrophage polarization markers, cytokine levels, and key proteins in the TLR signaling pathway were analyzed.

Main Results:

• Curcumin treatment significantly improved body weight, colon parameters, and histopathological damage in colitis mice.
• Curcumin modulated cytokine profiles, decreasing pro-inflammatory (IL-1β, IL-6, CCL-2) and increasing anti-inflammatory (IL-33, IL-10) cytokines.
• Curcumin suppressed M1 macrophage markers (iNOS, TLR4) and promoted M2 markers (CD206, CD163), while downregulating TLRs signaling pathway components (TLR2, TLR4, MyD88, NF-κB, p38MAPK, AP-1).

Conclusions:

• Curcumin exerts significant therapeutic effects in experimental colitis.
• The mechanism involves the regulation of M1/M2 macrophage polarization balance.
• Curcumin ameliorates colitis by modulating the TLRs signaling pathway, highlighting its potential as a novel therapeutic agent for UC.