Figure 6
From: Computational Prediction and Validation of BAHD1 as a Novel Molecule for UlcerativeColitis
An NF-κ B inhibitor blocked the effects caused by BAHD1repression in Caco-2 cells.
Caco-2 cells were pre-treated with PTN before exposure to the inflammatorymediators mixture (Mix). (A) PTN inhibited the activation of theNF-kB pathway: the phosphorylation of IKK α/β andIκBα decreased significantly at a concentration of30 μm with little effect on cell viability[Supplementary Fig. S6]. (B) The NF-κ B inhibitor PTNeliminated the phosphorylation difference of IKK,IκBα and NF-κ B p65 in theNC/siBAHD1-treated cell model. (C) PTN repressed the expression ofassociated inflammatory genes such as TNF-α, IL-6, IL-8 and CCL3in vitro. The values represent themean ± SEM of three independentexperiments. Representative blots of cell lysates are shown from at leastthree independent experiments.
