“…This excites the growth factor beta-activated kinase 1 (TAK1), which in turn generates activation of the IKK kinase complex. Such a complex promotes phosphorylation and degradation of IκB-α (Inhibitor kappa B-alpha), resulting in the dissociation and release of NF-κB p65, known as an important factor in regulating this highly expressed immune process in patients with IBD ( Trzeciak-Jędrzejczyk et al, 2017 ; Yao et al, 2017 ; Lu et al, 2018 ). The NF-κB p65 migrate to the nucleus of cells and downregulate or supra-regulate the expression genes associated with the transcription of different inflammatory mediators (IL-12, IL-18, IL-23, IL-6, IL-1β, IL-10, TNF-α, and prostaglandins), activator protein 1, granulocyte-macrophage colony-stimulating factor, intercellular adhesion molecules, and inflammatory enzymes (iNOS and COX) ( Yao et al, 2017 ; Ramos and Papadakis, 2019 ).…”