Figure 4
From: Computational Prediction and Validation of BAHD1 as a Novel Molecule for UlcerativeColitis
Associated inflammatory mediators were enhanced by BAHD1 deficiency invitro.
Four groups are involved here (NC = negative controlsiRNA-transfected group; NC+Mix = Caco-2 cell modelgroup; siBAHD1 = siBAHD1-transfected group;siBAHD1 + Mix = Caco-2 cellmodel pre-treated with siBAHD1). (A) Effects of BAHD1 repression onthe expression of proinflammatory factors (TNF-α, IL-6,IL-1β, IFN-β and IFN-γ) in the Caco-2cell model. (B) Detection of IL-6, IL-8 and MCP-1 secretion in cellculture supernatant by ELISA, the siBAHD1 group is reported as the foldincrease compared with the simple cell model. (C) BAHD1 inhibition inthe cell model influenced the mRNA levels of chemokines such as IL-8, CCL3,CCL4, CCL5, CX3CL1 and CXCL10. (D) Expression of the cell adhesionmolecules ICAM-1 and VCAM-1 displayed similar increasing trends in the cellmodel with siBAHD1 interference. (E) The expression of CXCL3 andCXCL5 did not show the predicted trend at the mRNA level. (F) COX-2and NO synthases, including iNOS and eNOS, showed higher expression in thecell model pre-treated with siBAHD1. All data above are shown as themean ± SEM from three independentmeasurements. Statistical significance was determined byStudent’s t-test(*P < 0.05;**P < 0.01). The western blots shown arerepresentative of at least three independent experiments.
