Cinnamon reduces inflammatory response in intestinal fibroblasts in vitro and in colitis in vivo leading to decreased fibrosis

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Abstract

Scope:

Intestinal fibrosis, a complication of inflammatory bowel disease, is currently being addressed by surgery alone, with no adequate alternative therapy available for patients. We propose that anti-inflammatory plant substances like cinnamon extract (CE) or its main compound cinnamaldeyde (CA) could aid in therapy. We recently found CE reducing inflammation in murine colitis. Here, we analyzed effects of CE on fibrosis in IL-10−/− colitis.

Methods and results:

IL-10−/− and wild-type (WT) mice were orally treated with/without vehicle or CE. Colonic tissue was analyzed for collagen deposition and expression of matrix metalloproteinases (MMPs). Influence of CE or CA on expression and release of cytokines, and phosphorylation of IκB in LPS-activated fibroblasts was assessed. Fibrosis score and mRNA expression of MMPs were down-regulated in colonic tissue of CE-treated IL-10−/− mice. Fibroblasts treated with CE or CA showed reduced expression and release of IL-6, KC/C-X-C motif ligand (CXCL) 8, and C-C motif ligand (CCL) 2 in response to LPS-treatment. CE and CA appear to act via reducing phosphorylation of IκB.

Conclusions:

Cinnamon decreases fibrotic symptoms and markers in murine colitis, and expression of inflammatory and fibrotic markers in hiFB. Thus, CE and CA could be potential anti-fibrotic agents in chronic colitis.

Treatment with cinnamon extract (CE) down-regulates fibrosis by reducing collagen deposition and expression of matrix metalloproteinases (MMP) in colonic tissue of IL-10-/- mice. Moreover, treatment with CE or its main compound cinnamaldeyde (CA) reduces expression of MMP-1 and the pro-inflammatory cytokines IL-6, KC/C-X-C motif ligand (CXCL) 8, and C-C- motif ligand (CCL) 2 in human intestinal fibroblasts (hiFB) in response to LPS.

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