Curcumin in inflammatory bowel diseases: Cellular targets and molecular mechanisms

Abstract

Curcumin, a natural product, has exhibited promising effects in both animal models and clinical trials, interacting with a multitude of factors linked to Inflammatory Bowel Disease (IBD). These factors encompass cytokines, oxidative stress-associated enzymes, and modulation of the intestinal microbiota. Notably, curcumin has demonstrated therapeutic potential in animal models of colitis, wherein it exerts a negative regulatory influence on pivotal signaling pathways such as PI3/Akt, JAK/STAT, and β-catenin. Moreover, it inhibits the expression of pro-inflammatory enzymes and co-stimulatory molecules (including RANKL, ICAM-1, CD205, CD256, TLR4, among others), while curbing immune cell chemotaxis, thereby attenuating the characteristic neutrophil infiltration observed in IBD. Another facet of curcumin’s action involves its modulation of the intestinal microbiota. Notably, the microbiota itself contributes to beneficial biotrans formations of curcumin, thereby enhancing its effectiveness in IBD treatment. On a clinical front, curcumin has demonstrated the ability to induce clinical and/or endoscopic remission without any reported toxic effects. Hence, curcumin warrants consideration as an adjunctive therapy in IBD management. Subsequent clinical investigations should concentrate on meticulously evaluating curcumin’s impact on these precise therapeutic targets.