Fig 1: Localization observation of phosphorylated NF-?B p65 (p-NF-?B p65), cyclooxygenase-2 (COX-2), tumor necrosis factor-a (TNF-a) and epidermal growth factor receptor (EGFR) expression in VP. (A) Immunohistochemical images of p-NF-?B p65, COX-2, TNF-a and EGFR of the prostate tissues in the rats treated using BPA, BPAF and PDTC (400×, scale bar = 20 µm). Arrows indicate the positive expression. Effect of exposure to BPA, BPAF and PDTC on the rate of positive expression of p-NF-?B p65 (B); the semiquantitative expression levels of COX-2 (C), TNF-a (D) and EGFR (E) in ventral prostate (VP). Results were performed as means ± SD, analyzed using ANOVA followed by LSD post hoc test, n = 8. Comparison of the individual administration group and the control: * p < 0.05, ** p < 0.01; comparison of the combined administration group and the individual administration group: # p < 0.05, ## p < 0.01.
Fig 2: TP treatment inhibited NF-?B–mediated prosurvival signals induced by TNF-a. (A) Time-dependent NF-?B activation induced by TNF-a (5 ng/ml). (B) Relative NF-?B activity induced by TP (25 nM) and TNF-a (5 ng/ml), 30 min after TNF-a treatment. (C–D) Representative western blots and relative intensity of protein bands of NF-?B p65 nuclear protein, with Lamin B1 as the loading control, 30 min after TNF-a (5 ng/ml) treatment. (E–H) Representative western blots and relative intensity of protein bands of CIAP1, CIAP2, XIAP, and FLIP in AGS and MKN45 cells treated with TP (25 nM) and TNF-a (5 ng/ml), 24 h after TNF-a application, with ß-actin as the loading control. Results were expressed as mean ± SEM, and statistical analysis was performed using one-way ANOVA or two-way ANOVA followed by Tukey’s multiple comparison test. *, # p < 0.05 (n = 3). *p compared with the control group and # p compared with the TNF-a-treated group.
Fig 3: BPA, BPAF and PDTC induced the quantitative changes of p-NF-?B p65, COX-2, TNF-a and EGFR in VP. Content of NF-?B p65 (A), COX-2 (B), TNF-a (C) and EGFR (D) was obtained using enzyme-linked immunosorbent assay (ELISA). Results are performed as means ± SD, analyzed using ANOVA followed by LSD post hoc test, n = 4. Comparison of the individual administration group and the control: * p < 0.05, ** p < 0.01; comparison of the combined administration group and the individual administration group: # p < 0.05, ## p < 0.01.
Fig 4: PDTC influenced BPA- and BPAF-facilitated NF-?B p65, COX-2, TNF-a and EGFR expression in prostate cells. Effect of exposure to BPA, BPAF and the inhibitor of NF-?B (PDTC) on the expression of NF-?B p65 (A), COX-2 (B), TNF-a (C) and EGFR (D) in WPMY-1 cells and the levels of NF-?B p65 (E), COX-2 (F) and EGFR (G) in HPrF cells. Results are performed as means ± SD, analyzed using ANOVA followed by LSD post hoc test, n = 3. Comparison of the individual administration group and the control: * p < 0.05, ** p < 0.01; comparison of the combined administration group and the individual administration group: # p < 0.05, ## p < 0.01.
Fig 5: Effects of GAN and MTX alone or in combination on (A) concentration of NF-?B/p65; (B) mRNA expression of E-cadherin; (C) mRNA expression of N-cadherin; (D) mRNA expression of survivin; (E) mRNA expression of Bcl-2. * p < 0.05, ** p < 0.01 and *** p < 0.001.
Supplier Page from Abcam for NF kappaB p65 ELISA Kit