Study summary · research use only
Resveratrol inhibits bile acid-induced gastric intestinal metaplasia via the PI3K/AKT/p-FoxO4 signalling pathway
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study used gastric cell lines and tissue arrays (species not specified) to examine the effect of resveratrol on bile-acid-induced gastric intestinal metaplasia via the PI3K/AKT/p-FoxO4 signaling pathway. The abstract reports that resveratrol reduced CDX2 expression in a time- and dose-dependent manner and increased FoxO4 activity, while chenodeoxycholic acid reduced FoxO4 activity; bioinformatics and chromatin-immunoprecipitation assays indicated FoxO4 could bind the CDX2 promoter. Resveratrol was reported to increase FoxO4 phosphorylation through the PI3K/AKT pathway, and ectopic FoxO4 expression suppressed chenodeoxycholic-acid-induced marker expression, with an inverse correlation observed between phospho-FoxO4 and CDX2 in tissue arrays.
Abstract
Gastric intestinal metaplasia (GIM) is the essential pre-malignancy of gastric cancer. Chronic inflammation and bile acid reflux are major contributing factors. As an intestinal development transcription factor, caudal-related homeobox 2 (CDX2) is key in GIM. Resveratrol has potential chemopreventive and anti-tumour effects. The aim of the study is to probe the effect of resveratrol in bile acid-induced GIM. We demonstrated that resveratrol could reduce CDX2 expression in a time- and dose-dependent manner in gastric cell lines. A Cignal Finder 45-Pathway Reporter Array and TranSignal Protein/DNA Array Kit verified that resveratrol could increase Forkhead box O4 (FoxO4) activity and that Chenodeoxycholic acid (CDCA) could reduce FoxO4 activity. Furthermore, bioinformatics analysis showed that FoxO4 could bind to the CDX2 promoter, and these conjectures were supported by chromatin-immunoprecipitation (ChIP) assays. Resveratrol can activate FoxO4 and decrease CDX2 expression by increasing phospho-FoxO4 nucleus trans-location. Resveratrol could increase FoxO4 phosphorylation through the PI3K/AKT pathway. Ectopic FoxO4 expression can up-regulate FoxO4 phosphorylation and suppress CDCA-induced GIM marker expression. Finally, we found a reverse correlation between p-FoxO4 and CDX2 in tissue arrays. This study validates that resveratrol could reduce bile acid-induced GIM through the PI3K/AKT/p-FoxO4 signalling pathway and has a potential reversing effect on GIM, especially that caused by bile acid reflux.
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