Butyrate improves recovery from experimental necrotizing enterocolitis by metabolite hesperetin through potential inhibition the PI3K-Akt pathway

文献类型： 外文期刊

第一作者： Gao, Yanan

作者： Gao, Yanan;Yang, Liting;Yao, Qianqian;Wang, Jiaqi;Zheng, Nan;Gao, Yanan;Yang, Liting;Yang, Liting

作者机构：

关键词： Butyrate; Necrotizing enterocolitis; Hesperetin; PI3K-Akt signaling pathway

期刊名称：BIOMEDICINE & PHARMACOTHERAPY （ 影响因子：6.9； 五年影响因子：6.8 ）

ISSN： 0753-3322

年卷期： 2024 年 176 卷

页码：

收录情况： SCI

摘要： Necrotizing enterocolitis (NEC) is one of the most common and serious intestinal illnesses in newborns and seriously affects their long-term prognosis and survival. Butyrate is a short-chain fatty acid that can relieve intestinal inflammation, but its mechanism of action is unclear. Results from an in vivo neonatal rat model has shown that butyrate caused an improved recovery from NEC. These protective effects were associated with the metabolite of hesperetin, as determined by metabolomics and molecular biological analysis. Furthermore, transcriptomics combined with inhibitor assays were used to investigate the mechanism of action of hesperetin in an in vitro NEC model (IEC-6 cells exposed to LPS) to further investigate the mechanism by which butyrate attenuates NEC. The transcriptomics analysis showed that the PI3K-Akt signaling pathway was involved in the antiNEC effect of hesperitin. Subsequently, the results using an inhibitor of PI3K (LY294002) indicated that the suppression could be explained by the hesperetin-induced expression of tight junction (TJ) proteins by potentially blocking the PI3K-Akt signaling pathway. In summary, the present study demonstrated that butyrate could improve recovery from NEC with a hesperetin metabolite, causing potential inhibition of the phosphorylation of the PI3K-Akt signaling pathway, resulting in the increased expression of TJ proteins. These findings reveal a potential new therapeutic pathway for the treatment of NEC.

分类号：

  • 相关文献
作者其他论文 更多>>

微信小程序