Fig 2: Combination of curcumin with HHT inhibit the growth of lymphoma cells via inhibition of VEGF/VEGFR2 signaling pathway. Raji cells were treated with 5 ng/mL HHT or/and 10 µM curcumin for 72 h or treated with HHT, curcumin and VEGF. The levels of (A) VEGF-A, (B) VEGF-B, (C) VEGF-C, (D) VEGF-D in cell culture supernatant was assessed with ELISA. (E) Expression levels of p-VEGFR2, VEGFR2, p-Akt, Akt, p-eNOS and eNOS in Raji cells were detected with western blotting. (E–H) The relative expressions of p-VEGFR2, p-Akt, and p-eNOS in cells were quantified via normalization to VEGFR2, Akt and eNOS. (I) Expression levels of p-p38, p38, p-HSP27, HSP27, p-ERK, ERK, p-JNK, JNK in Raji cells were detected with western blotting. (J–N) The relative expressions of p-p38, p-HSP27, p-ERK, p-JNK, JNK in cells were quantified via normalization to p38, HSP27, ERK, JNK and ß-actin. *P < 0.05, **P < 0.01 compared with control group; #P < 0.05, ##P < 0.01 compared with HHT group; ^P < 0.05, ^^P < 0.01 compared with HHT + curcumin group.

Fig 3: YB1 knockdown inhibits H2O2-induced phosphorylation of STAT3. H9c2 cells were transfected with siYB1 or siNC (as a control) for 24 h, and treated with H2O2 for 6 h. (A) YB1, p-P38, p-JNK, p-ERK1/2, p-P65, P38, JNK, ERK1/2 and P65 protein expression levels were detected using western blotting. (B) Relative expression levels of these proteins were calculated by normalizing to those of GAPDH, respectively. (C) Ratios of phosphorylated protein to total proteins after normalization to GAPDH furthers the observation these proteins are not recruited following treatment (D) YB1, p-JAK1, p-JAK2, p-STAT1, p-STAT3, JAK1, JAK2, STAT1 and STAT3 protein expression levels were detected using western blotting. (E) Relative expression levels of these proteins were calculated by normalizing to those of GAPDH. (F) Ratios of phosphorylated protein to total proteins after normalization to GAPDH demonstrates that STAT3 phosphorylation levels decrease in the absence of YB1 following treatment. Data are presented as the mean ± standard error of the mean (n=3). **P<0.01. YB1, Y-box protein 1; siYB1, small interfering RNA against YB1; siNC, scrambled small interfering RNA; p-, phosphorylated; JNK, c-Jun NH2-terminal kinase; ERK, extracellular signal-regulated kinase; JAK, Janus kinase; STAT, signal transducer and activator of transcription.

Fig 4: AKT and JNK Oppositely Regulate the Long-Term Glc Response in ESCs(A–D) Western blots on whole cell lysates or nuclear fractions as indicated.(E) Cells were immunostained for FOXO3a and counterstained with DAPI.(F) qPCR analysis for FOXO target genes determined with the 2-??Ct method and correction for PCR efficiency using Tbp as the housekeeper. n = 3 independent replicates ± SD.(G) Percentage of cells in cell-cycle stages were measured with flow cytometry using propidium iodide-treated cells and S/G1 ratios calculated. n = 3 independent replicates ± SD.(H and I) SOD (H) and CAT (I) activity is increased in AKT-inhibited cells, similar to cells exposed to 25 mM Glc alone. n = 5 independent replicates ± SD.(J) Superoxide anion levels. n = 5 ± SD.(K) Hydrogen peroxide levels. n = 5 independent replicates ± SD.*p < 0.05, one-way ANOVA versus 5.5 mM Glc; ?p < 0.05, one-way ANOVA versus 25 mM Glc. 124005, AKT inhibitor; CAT, catalase; DHR, dihydrorhodamine; Glc, glucose; GSH-OEt, glutathione reduced ethyl ester; RLU, relative light units; SOD, superoxide dismutase; TBP, TATA binding protein; UT, untreated.

Fig 5: Effect of protocatechuic acid (PCA) on the CXCL1 mRNA and protein level in glial satellite cells treated by tumor necrosis factor (TNF)-a. Glial satellite cells induced by TNF-a were treated with simvastatin, PCA (20 or 50 µM), SP600125 (a inhibitor of the JNK pathway), U0126 (a inhibitor of the ERK pathway) or SB203580 (a inhibitors of the p38/MAPK pathway). Reverse transcription quantitative polymerase chain reaction and Western blot assays were used to detect the CXCL1 mRNA level (A-C) or protein level (D and E) in glial satellite cells. **p<0.01 versus TNF-a (-) group, #p<0.05 versus TNF-a (+) group, &p<0.05 versus TNF-a (+) group treated with simvastatin, 50 µM PCA or SP600125.