Abstract
Although Aster glehni is a common dietary herb that has various bioactivities, including anti-diabetic, anti-adipogenic, and anti-inflammatory effects, A. glehni has not been studied in colon cancer. Therefore, we hypothesized the chemopreventive effects of an ethanol extract of A. glehni (AG) on azoxymethane/dextran sulfate sodium (AOM/DSS)-induced colitis-associated cancer (CAC) in mice. In this study, we found that treatment with AG significantly attenuated the AOM/DSS-induced enlargement of the spleen and shortening of the colon. In addition, colonic tumor formation, colonic damage, and increased muscle thickness were significantly reduced in AOM/DSS-induced mice fed AG. Treatment with AG also reduced intestinal interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α production and decreased inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 protein expression in mice with AOM/DSS-induced CAC. Furthermore, AG reduced nuclear factor (NF)-κB activation via phosphorylation and degradation of inhibitor of kappa Bα (IκBα), leading to inhibition of NF-κB p65 nuclear translocation. It also downregulated the expression of NF-κB-related proteins, including the B-cell lymphoma 2 (Bcl-2) family and inhibitors of apoptosis proteins (IAPs), in mice with AOM/DSS-induced CAC. Taken together, these findings suggest that the treatment with AG inhibited colitis-associated colon carcinogenesis in mice, and this chemopreventive effect was strongly mediated by suppression of the NF-κB signaling pathway, indicating that AG could be a promising protective agent against CAC.
Highlights
Inflammatory bowel disease (IBD) refers to a group of chronic dysregulated inflammatory conditions in the large and small intestine of humans, and it is well known that chronic inflammation in the colon can lead to cancer [1]
It is well known that chronic including a diet low in fruits, fiber, vegetables, and high in chronic animal IBD, fat and other high-calorie inflammation plays a critical roleand in colon carcinogenesis, with such as ulcerative colitisfoods, contribute to the disease, development of colorectal cancer (CRC)
COX-2 is upregulated protein responsible for the overproduction of prostaglandins in inflammation contributing to the progression of IBD. inducible nitric oxide synthase (iNOS) activation lead to excessive production of NO, which causes DNA damage and inhibits the DNA repair process [19]
Summary
Inflammatory bowel disease (IBD) refers to a group of chronic dysregulated inflammatory conditions in the large and small intestine of humans, and it is well known that chronic inflammation in the colon can lead to cancer [1]. Colitis-associated cancer (CAC), the colorectal cancer (CRC). CRC is caused by the accumulation of mutations in oncogenes and tumor suppressor genes. Mutations in the adenomatous polyposis coli (APC) oncogene-related pathway mediate the transition of single preneoplastic cells to aberrant crypt foci (ACF), and to adenoma and colorectal carcinoma [4]. Chronic inflammation, which leads to CAC, is characterized by the production of pro-inflammatory cytokines. These can induce mutations in oncogenes and tumor
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