Fig 1: Modulation of Cytokines by iAs during Skin Carcinogenesis, as Modulated by BTE. (a) Levels of cytokines, TNF-α, IL-2, IL-6, IL-8, IL-10, IL-13, IL-17a, IL-22 as assessed by ELISA have been depicted as bar diagram. Values are mean of three independent experiments and are significant at *p<0.0001, with respect to the control value. Modulation of cytokine levels by BTE, with respect to the treated group is significant at ap<0.0001, bp<.001, cp<0.05. (b) Expression levels of TNF-α, IL-2, IL-6, IL-8, IL-10, IL-13, IL-17a, IL-22, as altered by iAs and modulated by BTE have been shown. Lanes 1, 2, 3 signify control, iAs and iAs+BTE treated groups respectively
Fig 2: Role of Jian Gan powder (JGP) in BCG + LPS-induced immunological liver injury (ILI) in BALB/c mice. A Experimental schedule. B ELISA of the serum levels of interferon-gamma (IFN-γ), interleukin (IL)-6, IL-10, and IL-22. C Western blotting analysis of STAT3 and p-STAT3 protein levels in the liver of experimental and control groups (five mice per group). D Representative images of proliferating cell nuclear antigen (PCNA) staining (× 200) and the percentage of PCNA-positive cells (arrowhead). (A normal group; B model group [induced for experimental ILI]; C positive control group; D JGP-L group; E: JGP-M group; F: JGP-H group). Bars: 100 μm. Data were analyzed using one-way analysis of variance and were presented as mean ± SEM. #p < 0.05, ##p < 0.01, ###p < 0.001; *p < 0.05, **p < 0.01, ***p < 0.001
Fig 3: Effects of ISDF on inflammatory response induced by IMQ in mice. A Serum levels of IL-17A, IL-22 and IL-6. B Skin levels of IL-17A, IL-22 and IL-4. C Gene expression of IL-4, IL-6, IL-1β and TNF. D, E Protein expression of NF-κB and MAPK pathways. D Western blotting bands. E Results of quantitative analysis. Data were presented as mean ± SEM (n = 8). *p < 0.05 and **p < 0.01 compared with the IMQ group
Fig 4: Effects of ISDF on inflammatory response induced by IL-23 in mice. A Serum levels of IL-17A and IL-22, and the level of IL-23 in the injected skin. B, C Protein expression of Jak/Stat3 pathways. B Results of quantitative analysis. C Western blotting bands. Data were presented as mean ± SEM (n = 8). *p < 0.05 and **p < 0.01 compared with the IL-23 group
Fig 5: Inhibition of inflammation reduces embryonic developmental defects in Pgrd/d mice.(A) Diagram of the carprofen (40 mg/kg) treatment during preimplantation embryonic development in vivo. (B) Representative images (scale bars, 100 μm) and (C) quantification of embryos collected from the reproductive tract of Pgrf/f and Pgrd/d mice at 3.5 dpc after the treatment of carprofen; n = 4 to 6 mice per treatment per genotype. *P < 0.05 and **P < 0.01, respectively, compared to the corresponding genotype without carprofen. (D) ELISA analyses of IL-22 and TLR4 in the oviduct after the treatment of carprofen. (E) Representative images (scale bars, 100 μm) and (F) quantification of WT embryos cultured with PBS or recombinant IL-22 (50 pg/ml) from zygote stage (day 1 culture) until blastocyst stage (day 5 culture); n = zygotes from at least 24 mice per treatment. **P < 0.01 compared to PBS. All images are taken at ×200 magnification. All data are represented as means ± SEM.
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