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. 2015 Dec 9;16(12):29370–29382. doi: 10.3390/ijms161226174

Figure 4.

Figure 4

Resistin-initiated HCT-116 adhesion to HUVECs is mediated by NF-κB activation. (A) and (C) HCT-116 cells were maintained as control or stimulated with resistin for 1, 2, and 4 h and then NF-κB activation (A) and p65 phosphorylation (C) were determined by ELISA kit and Western blot, respectively; (B,D,E) HCT-116 cells were pretreated with (B,D) DMSO or NF-κB inhibitors (PDTC or SN50) and (E) control or p65 specific siRNA and then stimulated with resistin. HCT-116 cell adhesion and ICAM-1/VCAM-1 mRNA expression were analyzed. Data represent the mean ± SEM from three independent experiments. * p < 0.05 vs. control cells; # p < 0.05 vs. DMSO or si-CL cells with resistin treatment; § p < 0.05 vs. PDTC, SN50, or si-p65 cells without resistin treatment.