Fig 2: Microtubule network damage influences the visfatin catabolic effect on COX2 upregulation in human primary chondrocytes. Human primary chondrocytes were pretreated with DMSO, phalloidin (microfilament stabilizer, 3 µM), or paclitaxel (microtubule stabilizer, 1 µM) for 1 h and then kept as controls (CL) or treated with 5 µg/mL of visfatin (Vis) for 8 h. COX2 expression and GSK3ß-Ser9 phosphorylation in human primary chondrocytes were analyzed by Western blot. Results are representative of three independent experiments with similar results. Statistic data are mean ± SEM from three independent experiments. *, p < 0.05 vs. DMSO-CL-treated cells. #, p < 0.05 vs. DMSO-visfatin (Vis)-stimulated cells.

Fig 3: p38 signaling regulates the effect of visfatin on GSK3ß inactivation and subsequent COX2 expression in human primary chondrocytes. (A) Human primary chondrocytes were kept as controls (CL) or treated with 5 µg/mL of visfatin for 1, 4, 8 and 24 h, and then the p38-Thr180/Tyr182 and ERK1/2-Thr202/Tyr204 kinases phosphorylations were analyzed by Western blot. (B,C) Human primary chondrocytes were pretreated with DMSO, PD98059 (ERK1/2 inhibitor, 30 µM), or SB203580 (p38 inhibitor, 10 µM) for 1 h and then kept as controls (CL) or treated with 5 µg/mL of visfatin (Vis) for 8 h. COX2 expression (B) and GSK3ß-Ser-9 phosphorylation (C) in human primary chondrocytes were analyzed by Western blot. Results in (A–C) are representative of three independent experiments with similar results. Statistic data in (A–C) are mean ± SEM from three independent experiments. *, p < 0.05 vs. untreated control cells (CL) or DMSO-CL-treated cells. #, p < 0.05 vs. DMSO-visfatin (Vis)-stimulated cells.

Fig 4: Effect of RFX on prognostic markers of cancer progression in ER+ mammary gland cancer. Immunoblotting of respective individual group control (1), toxic control (MNU, 47 mg kg-1) (2), RFX (25 mg kg-1) (3) and RFX (50 mg kg-1) (4) were subjected for UCHL-1 and COX-2. ß-Actin was used as internal loading control. Each experiment was performed in triplicate. The data were represented as mean ± SD. Comparisons were made on the basis of the one-way ANOVA followed by Bonferroni multiple test. All groups were compared to the toxic control and control groups (*/ap < 0.05, **/bp < 0.01, ***/cp < 0.001).

Fig 5: Rat muscle without notexin (control, C and foam rolling, FR) or with notexin (notexin, N and notexin with foam rolling, NFR) was collected to determine (a) PPAR-? and (b) COX-2 protein expression. Data are shown as the median for the group with error bars indicting the 95% confidence interval (N=5).*p < 0.05 vs. control. #p < 0.05 vs. notexin.