Abstract
Inflammatory bowel disease (IBD) is a major risk factor of colorectal cancer. Drugs currently used for IBD exhibit adverse effects including vomiting, nausea, and diarrhea. Naturally derived novel alternative therapies are required to overcome these limitations. In this study, we investigated the protective effects of ethanol extract of Cicer arietinum (CEE) in a dextran sodium sulfate (DSS)-induced mouse model of colitis. CEE markedly improved DSS-induced clinical symptoms and histological status, such as the disease activity index, spleen weight, and colon length. Moreover, CEE-treated mice showed significant recovery of DSS-induced crypt damage and cell death. CEE suppressed myeloperoxidase (MPO) activity and macrophage marker F4/80 mRNA expression in colonic tissue of mice with DSS-induced colitis, indicating neutrophil infiltration and macrophage accumulation, respectively. Although DSS upregulated pro-inflammatory mediators and activated transcription factors, CEE downregulated the mRNA expression of cytokines including interleukin-6, interleukin-1β, and tumor necrosis factor-α, protein expression of cyclooxygenase-2 and inducible nitric oxide synthase, as well as activation of nuclear factor-kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3). Hence, our findings reveal that the anti-inflammatory properties of CEE, involving the downregulation of the expression of pro-inflammatory mediators by inactivating NF-κB and STAT3 in DSS-induced colitis mice.
Highlights
The integrity of the epithelial barrier is crucial for intestinal homeostasis
signal transducer and activator of transcription 3 (STAT3) phosphorylation in colonic tissue (Figure 6B). These results indicated that Cicer arietinum (CEE) exerted an anti-colitis effect through the suppression of inflammatory protein expression by interfering with the NF-κB and STAT3 activation in colon tissue from dextran sodium sulfate (DSS)-treated mice
We showed that oral administration of CEE
Summary
The integrity of the epithelial barrier is crucial for intestinal homeostasis. Barrier integrity disruption leads to an abnormal immune response and results in autoimmune conditions, including inflammatory bowel disease (IBD) [1]. Nutrients 2020, 12, 456 uncontrolled inflammatory response, including ulcerative colitis (UC) and Crohn’s disease [2]. UC is related to genetic factors, environmental factors, infection, dysbacteriosis, and immune factors, the pathogenesis of UC is still unclear [4]. Among those factors, the immune component involving cytokine-driven mixed inflammatory infiltrate in the intestinal mucosa is the most widely accepted factor that has been investigated [5]
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