Cherry Polyphenol Extract Ameliorated Dextran Sodium Sulfate-Induced Ulcerative Colitis in Mice by Suppressing Wnt/β-Catenin Signaling Pathway

Abstract

Ulcerative colitis (UC) is a chronic and nonspecific inflammatory disease of the colon and rectum, and its etiology remains obscure. Cherry polyphenols showed potential health-promoting effects. However, both the protective effect and mechanism of cherry polyphenols on UC are still unclear. This study aimed to investigate the potential role of the free polyphenol extract of cherry in alleviating UC and its possible mechanism of action. Our study revealed that the free polyphenol extract of cherry management significantly alleviated UC symptoms, such as weight loss, colon shortening, the thickening of colonic mucous layer, etc. The free polyphenol extract of cherry treatment also introduced a significant reduction in levels of malondialdehyde (MDA), myeloperoxidase (MPO) and nitric oxide (NO), while causing a significant elevation in levels of catalase (CAT), glutathione (GSH-Px), superoxide dismutase (SOD), as well as the downregulation of pro-inflammatory cytokines. This indicated that such positive effects were performed through reducing oxidative damage or in a cytokine-specific manner. The immunofluorescence analysis of ZO-1 and occludin proteins declared that the free polyphenol extract of cherry had the potential to prompt intestinal barrier function. The reduced expression levels of β-catenin, c-myc, cyclin D1 and GSK-3β suggested that the cherry extract performed its positive effect on UC by suppressing the Wnt/β-ctenin pathway. This finding may pave the way into further understanding the mechanism of cherry polyphenols ameliorating ulcerative colitis.

Schisandrin A Suppresses Inflammation in DSS-induced IBD Mice and H2O2-induced MODE-K Cells through Wnt/β-Catenin Signaling

“…The expression of β-catenin was highly correlated with UC progression. In colonic mucosa damaged, β-catenin accumulates and is translocated into the nuclear compartment, which transcriptionally activates cell-proliferation-associated genes (c-Myc and cyclin D1), exacerbating UC (Li et al, 2021). As demonstrated above, Wnt3a and β-catenin amounts in DSS-induced IBD mice were starkly increased and then significantly decreased after administration of SchA, corroborating previously reported findings.…”

Phenolics from Dendrobium officinale Leaf Ameliorate Dextran Sulfate Sodium-Induced Chronic Colitis by Regulating Gut Microbiota and Intestinal Barrier

“…Mice in the SASP, DOPL, and DOPH groups were gavaged with 50 mg/kg body weight (BW) SASP, 150 mg/kg BW DOP, and 450 mg/kg BW DOP daily. The selection of dosage was examined in the previously published literature, , and a detailed explanation of justification can be found in the Supporting Information.…”

Preventive effect of tilapia skin collagen hydrolysates on ulcerative colitis mice based on metabonomic and 16 S rRNA gene sequencing

“…It is primarily prevalent in Western countries, especially in North America, Europe, and Oceania; however, its prevalence in developing countries is increasing, causing an economic burden on society 9‐12 . The pathogenesis of UC is multifaced; genetics, the environment, microbiota, and dysregulated immune responses all contribute, but its underlying pathogenesis remains unclear 13‐15 . At present, salicylates (sulfasalazine), corticosteroids (prednisolone), immunosuppressive agents [cyclosporin A and tacrolimus (FK506)], tumor necrosis factor (TNF) antagonists (infliximab, adalimumab, golimumab), integrin blockers, and interleukin (IL) antagonists are the main drugs for ameliorating inflammation in UC in the clinic; however, they are affiliated with a range of side‐effects, which has restricted them as inadequate for frequent use 16‐18 .…”

“…[9][10][11][12] The pathogenesis of UC is multifaced; genetics, the environment, microbiota, and dysregulated immune responses all contribute, but its underlying pathogenesis remains unclear. [13][14][15] At present, salicylates (sulfasalazine), corticosteroids (prednisolone), immunosuppressive agents [cyclosporin A and tacrolimus (FK506)], tumor necrosis factor (TNF) antagonists (infliximab, adalimumab, golimumab), integrin blockers, and interleukin (IL) antagonists are the main drugs for ameliorating inflammation in UC in the clinic; however, they are affiliated with a range of side-effects, which has restricted them as inadequate for frequent use. [16][17][18] Therefore, it is of great significance and urgency to identify new active substances with low toxicity, high effectiveness, and cost-effective.…”