Baicalin Magnesium Salt Attenuates Lipopolysaccharide-Induced Acute Lung Injury via Inhibiting of TLR4/NF-κB Signaling Pathway

Figure 7

Regulation of LPS-induced TLR4/NF-κB signaling pathway by ubiquitination and phosphorylation. When NF-κB is not subjected to external stimulation, it can induce the assembly of an inactive IκB/p50/p65 trimer. After LPS stimulation, the activated TLR4 firstly forms a complex with MyD88. Then, the MyD88 complex promotes the phosphorylation of IRAK4, thereby further phosphorylates TRAF6, while detaching from MyD88. Ubiquitination of TRAF6 induces downstream IKK-mediated NF-κB signaling pathway, triggering downstream IκB phosphorylation and inactivation, which leads to NF-κB dimer breaking away from IκB, thereby entering the nucleus and acting on the original NF-κB response element, that is, the gene locus of binding to NF-κB. Thereafter, the transcriptional translation process is initiated, which leads to the expression of downstream genes related to inflammatory factors and chemokines.