Fig 1: Effect of astaxanthin on autoinflammatory gene expression in RAW 264.7 cells. (A) Schematic representation of experimental procedures. Cells were seeded the same as for the inflammatory gene expression experiments and treated with astaxanthin or DMSO for 24 h, but with no further treatment with CML-HSA, to measure the autoinflammatory gene expression by qPCR. Expression was analyzed based on mRNA levels of (B) TNFa, (C) IL-1ß, (D) IL-6, (E) iNOS, (F) NFATc1, (G) c-Fos, and (H) RAGE. All data were normalized using GAPDH and are shown as the mean ± SEM (n = 3) of the ratios against no treatment. * p < 0.05, ns denoted not significant by Tukey–Kramer test. DMSO, dimethyl sulfoxide; TNF, tumor necrosis factor; IL, interleukin; iNOS, inducible nitric oxide synthase; RAGE, receptor for advanced glycation end products; NFATc1, nuclear factor of activated T-cell, cytoplasmic 1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; SEM, standard error mean.
Fig 2: The tumor level of the TNF-ain EST-bearing mice treated with 10-HDA alone and in combination with cyclophosphamide (CP). Non-EST and non-treated mice (C1); EST mice receiving the normal saline (C2); EST mice treated with CP (50 mg/kg) intraperitoneally once a day for 3 days (C3); EST mice treated with 10-HDA 2.5 mg/kg orally once a day for 2 weeks (E1); EST mice treated with 10-HDA 5 mg/kg orally once a day for 2 weeks (E2); EST mice treated with 10-HDA 2.5 mg/kg + CP (25 mg/kg) once a day for 2 weeks (E3); EST mice treated with 10-HDA 5 mg/kg + CP (25 mg/kg) once a day for 2 weeks (E3). Data are expressed as the mean ± SD (n = 3). * p < 0.001 significant difference compared with C2 group; + p < 0.001 significant difference compared with C3 group.
Fig 3: Tea treatments alleviate major liver inflammatory cytokines and redox state in liver: (a) liver IL-6; (b) liver TNF-alpha content; (c) liver MDA content; (d) liver SOD activity. Data were expressed as mean ± SEM. (a–c) Analysis of variance (ANOVA) and Tukey multiple comparison (n = 7). Differences of data (d) were assessed by Kruskal-Wallis test with Dunn's multiple comparison test, respectively (n = 7). *p < 0.05, **p < 0.01 compared with the HFD group. #p < 0.05, ##p < 0.01 compared with the NFD group.
Fig 4: Effects of lncRNA-MM2P on the expression of pro-inflammatory cytokines in the supernatants of MSU-induced cells. The mRNA expression of inflammatory cytokines, (A) IL-1ß, (B) IL-8 and (C) TNFa, increased in the supernatants of RAW 264.7 cells after MSU treatment, and these effects were more notable when lncRNA-MM2P-1 was knocked down in cells. The mRNA expression of inflammatory cytokines, (D) IL-1ß, (E) IL-8 and (F) TNFa, increased in the supernatant of THP-1 cells after MSU treatment, and these effects were more notable when lncRNA-MM2P-1 was knocked down in cells. The mRNA expression of inflammatory cytokines, (G) IL-1ß, (H) IL-8 and (I) TNFa, increased in the supernatant of RAW 264.7 cells after MSU treatment, and these effects were reversed in lncRNA-MM2P-1 overexpressing cells. The mRNA expression of inflammatory cytokines, (J) IL-1ß, (K) IL-8 and (L) TNFa, increased in the supernatant of THP-1 cells after MSU treatment, and these effects were reversed in lncRNA-MM2P-1 overexpressing cells. *P<0.05, **P<0.01. lncRNA, long non-coding RNA; MSU, monosodium urate; IL, interleukin; TNF, tumor necrosis factor; ns, not significant.
Fig 5: Effect of MSU treatment on the expression of pro-inflammatory cytokines. The mRNA expression levels of inflammatory cytokines, (A) IL-1ß, (B) IL-8 and (C) TNFa, were upregulated in RAW 264.7 cells as the concentration of MSU increased. The mRNA expression levels of inflammatory cytokines, (D) IL-1ß, (E) IL-8 and (F) TNFa, were upregulated in THP-1 cells as the concentration of MSU increased. *P<0.05, **P<0.01 vs. 0. MSU, monosodium urate; IL, interleukin; TNF, tumor necrosis factor; ns, not significant.
Supplier Page from Abcam for Mouse TNF alpha ELISA Kit