Abstract:
:An impaired gut-liver axis is a potential factor that contributes to alcoholic liver disease. Specifically, ethanol decreases intestinal integrity and causes gut dysbiosis. Butyrate, a fermentation byproduct of gut microbiota, is negatively altered following acute ethanol exposure. This study aimed to determine whether kaempferol could protect against alcoholic liver injury (AALI) in mice by regulating tight junction (TJ) proteins and butyrate receptors and transporters in intestines. Male Institute of Cancer Research (ICR) mice were randomly divided into five treatment groups: control, ethanol administered (5 g/kg), and the low-, medium- and high-dosage kaempferol (25, 50, 100 mg/kg) treatments. Intestinal expression was evaluated for the TJ proteins ZO-1 and occludin and the butyrate receptor GPR109A and butyrate transporter SLC58A proteins, in addition to plasma ALT and AST levels and pathomorphological changes in liver and intestinal tissues. The expression of the TJ proteins ZO-1 and occludin, butyrate receptors, and butyrate transporters in the ileum and proximal colon decreased in AALI mice, while plasma ALT and AST levels markedly increased. Kaempferol supplementation reversed these effects. These results suggest that kaempferol could serve as a prophylactic treatment against AALI in mice by increasing the expression of butyrate receptors, transporters, and TJ proteins in the intestinal mucosa.
journal_name
Toxicologyjournal_title
Toxicologyauthors
Chen J,Xuan YH,Luo MX,Ni XG,Ling LQ,Hu SJ,Chen JQ,Xu JY,Jiang LY,Si WZ,Xu L,Gao H,Liu Z,Li Hdoi
10.1016/j.tox.2019.152338subject
Has Abstractpub_date
2020-01-15 00:00:00pages
152338eissn
0300-483Xissn
1879-3185pii
S0300-483X(19)30295-1journal_volume
429pub_type
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