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

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.