Genistein inhibits AOM/DSS-induced colon cancer by regulating lipid droplet accumulation and the SIRT1/FOXO3a pathway in high-fat diet-fed female mice

Qi, Wentao; Wang, Yong; Yao, Jianquan; Sun, Haixiang; Duan, Xiaoliang; Song, Ge; Pang, Shaojie; Li, Aike

doi:10.1080/09540105.2019.1684452

Cited by 5 publications

(3 citation statements)

References 40 publications

(44 reference statements)

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“…The total protein concentration of colonic mucosal samples was determined using the BCA protein assay kit (Tiangen Biotech, Beijing, China). Western blot analysis was performed according to our previous study [22]. In brief, an equal amount of protein from each group was separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and transferred to nitrocellulose (NC) membranes (Millipore, Bedford, MA, USA).…”

Section: Experimental Designmentioning

confidence: 99%

High-Fructose Diet Increases Inflammatory Cytokines and Alters Gut Microbiota Composition in Rats

Wang

Song

et al. 2020

Mediators of Inflammation

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High-fructose diet induced changes in gut microbiota structure and function, which have been linked to inflammatory response. However, the effect of small or appropriate doses of fructose on gut microbiota and inflammatory cytokines is not fully understood. Hence, the abundance changes of gut microbiota in fructose-treated Sprague-Dawley rats were analyzed by 16S rRNA sequencing. The effects of fructose diet on metabolic disorders were evaluated by blood biochemical parameter test, histological analysis, short-chain fatty acid (SCFA) analysis, ELISA analysis, and Western blot. Rats were intragastrically administered with pure fructose at the dose of 0 (Con), 2.6 (Fru-L), 5.3 (Fru-M), and 10.5 g/kg/day (Fru-H) for 20 weeks. The results showed that there were 36.5% increase of uric acid level in the Fru-H group when compared with the Con group. The serum proinflammatory cytokines (IL-6, TNF-α, and MIP-2) were significantly increased ( P < 0.05 ), and the anti-inflammatory cytokine IL-10 was significantly decreased ( P < 0.05 ) with fructose treatment. A higher fructose intake induced lipid accumulation in the liver and inflammatory cell infiltration in the pancreas and colon and increased the abundances of Lachnospira, Parasutterella, Marvinbryantia, and Blantia in colonic contents. Fructose intake increased the expressions of lipid accumulation proteins including perilipin-1, ADRP, and Tip-47 in the colon. Moreover, the higher level intake of fructose impaired intestinal barrier function due to the decrease of the expression of tight junction proteins (ZO-1 and occludin). In summary, there were no negative effects on body weight, fasting blood glucose, gut microbiota, and SCFAs in colonic contents of rats when fructose intake is in small or appropriate doses. High intake of fructose can increase uric acid, proinflammatory cytokines, intestinal permeability, and lipid accumulation in the liver and induce inflammatory response in the pancreas and colon.

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Section: Experimental Designmentioning

confidence: 99%

High-Fructose Diet Increases Inflammatory Cytokines and Alters Gut Microbiota Composition in Rats

Wang

Song

et al. 2020

Mediators of Inflammation

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“…Another study reported the beneficial effects against DSS-induced colitis were achieved via ubiquitination of NLRP3 inflammasome [167]. Furthermore, the anti-tumor effects were also reported in AOM/DSS-induced CRC in high-fat mice through the PI3K/AKT/FOXO3 or SIRT1/FOXO3 signal cascades [168,169]. Moreover, individual supplementation with genistein or combined with hesperidin in feed was reported to attenuate LPS-induced inflammatory responses and mucosal damage in the small intestines of broilers [153].…”

Section: Interventional Options Of Polyphenols In Inflammation-relate...mentioning

confidence: 96%

New Insights of Biological Functions of Natural Polyphenols in Inflammatory Intestinal Diseases

Zhang

Deng

et al. 2023

IJMS

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The intestine is critically crucial for nutrient absorption and host defense against exogenous stimuli. Inflammation-related intestinal diseases, including enteritis, inflammatory bowel disease (IBD), and colorectal cancer (CRC), are heavy burdens for human beings due to their high incidence and devastating clinical symptoms. Current studies have confirmed that inflammatory responses, along with oxidative stress and dysbiosis as critical pathogenesis, are involved in most intestinal diseases. Polyphenols are secondary metabolites derived from plants, which possess convincible anti-oxidative and anti-inflammatory properties, as well as regulation of intestinal microbiome, indicating the potential applications in enterocolitis and CRC. Actually, accumulating studies based on the biological functions of polyphenols have been performed to investigate the functional roles and underlying mechanisms over the last few decades. Based on the mounting evidence of literature, the objective of this review is to outline the current research progress regarding the category, biological functions, and metabolism of polyphenols within the intestine, as well as applications for the prevention and treatment of intestinal diseases, which might provide ever-expanding new insights for the utilization of natural polyphenols.

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“…Studies of this flavonoid in animal models show its benefits to combat CRC, thus, an in-vivo study using AOM as chemical inducer of colon cancer in male Sprague-Dawley rats showed that rats fed 140 mg genistein/kg body weight since gestation until 13 weeks of age showed downregulation of Wnt/βcatenin and reduction in the total number of aberrant crypts (Zhang et al, 2013). Likewise, genistein inhibits AOM/DSS-induced colon cancer by regulating the accumulation of lipid droplets and the SIRT1/FOXO3a pathway in female mice fed with a diet rich in fats containing 250 ppm of genistein for 52 weeks (Qi et al, 2019). Xiao et al (2015), in an orthotopic implantation model of human CRC cells in mice, demonstrated that oral genistein did not inhibit tumor growth, but did inhibit metastasis formation; at cellular level, genistein inhibited the vascular endothelial growth factor receptor (FLT4) and metalloproteinase 2; FLT4 is a marker of metastatic disease and response to small molecule therapies that inhibit CRC metastasis.…”

Section: Genisteinmentioning

confidence: 99%

Phytochemicals and colorectal cancer: About polyphenols

Guerrero Ospina,

Restrepo,

Loango

et al. 2024

BLACPMA

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Dietary consumption of polyphenols, found in fruits and vegetables, has been associated with a potentially protective role in colorectal cancer (CRC). To establish the state of knowledge regarding advances in polyphenols, CCR and action mechanisms a systematic review and an analysis of information available until 2021 were made. Results indicate that only some polyphenols have in vitro, preclinical and clinical studies. These studies showed that polyphenols will inhibit human CRC cell invasion, migration, metastasis formation, tumor growth. Action mechanisms involve signaling pathways that modulate genes, proteins, markers or cell death inductors, like the AMPK pathway, caspases, Bcl-2, p-Akt, and NF-kB, lysosomal and mitochondrial dysfunction, cellular cycle arrest, among the best known and implied in CRC. Overall, in vitro, preclinical and clinical data on phytochemicals against CRC are still not sufficient and therefore the preventive or therapeutic impacts of dietary phytochemicals on CRC development deserve further research.

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Genistein inhibits AOM/DSS-induced colon cancer by regulating lipid droplet accumulation and the SIRT1/FOXO3a pathway in high-fat diet-fed female mice

Cited by 5 publications

References 40 publications

High-Fructose Diet Increases Inflammatory Cytokines and Alters Gut Microbiota Composition in Rats

High-Fructose Diet Increases Inflammatory Cytokines and Alters Gut Microbiota Composition in Rats

New Insights of Biological Functions of Natural Polyphenols in Inflammatory Intestinal Diseases

Phytochemicals and colorectal cancer: About polyphenols

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