Inhibition of TLR4 Suppresses the Inflammatory Response in Inflammatory Bowel Disease (IBD) by Modulating the PDK1-Induced Metabolism Reprogramming via a m6A-Denpendent Manner

抑制TLR4可通过m6A依赖的方式调节PDK1诱导的代谢重编程,从而抑制炎症性肠病(IBD)中的炎症反应。

阅读:1

Abstract

OBJECTIVE: To investigate the role of TLR4 and PDK1 genes in IBD. METHODS: The DSS mouse model was established by inducing BALB/C with 5% DSS solution. The behavior of DSS mice was detected, and the m6A modification was detected by m6A methylation chip. At the same time, the expressions of TLR and PDK1 were detected by fluorescence real-time quantitative PCR. RESULTS: The results showed that the model of dextran sodium sulfate colitis in mice was successful, and the colon membrane of mice had obvious naked eye inflammation. Through comparison, it was found that there were differences in m6A modification between the blank group and the model group, and compared with the blank group, the expression of PKD1 in DSS group was significantly reduced and the expression of TLR4 was significantly increased. CONCLUSION: TLR4 inhibition inhibits the inflammatory response in inflammatory bowel disease (IBD) in a m6A-dependent manner by regulating PDK1-induced metabolic reprogramming.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。