Fig. 7
From: A drug-free nanozyme for mitigating oxidative stress and inflammatory bowel disease
CeNP-PEG exerted a therapeutic effect on colitis model mice by ameliorating the hostile proinflammatory microenvironment. A Flow cytometric analysis of proinflammatory macrophages (CD11b+ CD86+) isolated from colonic tissues on day 9 after different treatments. B Quantified percentages of proinflammatory macrophages (n = 3). Proinflamm. MΦ: Proinflammatory macrophage. C Flow cytometric analysis of Th1 cells (CD4+ IFN-γ+) isolated from colonic tissues on day 9 after treatment. D Quantified percentages of Th1 cells (n = 3). E Flow cytometric analysis of Th17 cells (CD4+ IL-17A+) isolated from colonic tissues on day 9 after treatment. F Quantified percentages of Th17 cells (n = 3). G Western blotting analysis of key proteins in the NF-κB and JAK2/STAT3 signaling pathways on day 9 after treatmengt. H Proposed signaling pathways of self-perpetuation of proinflammatory microenvironment in IBD. The extravasated gut microbiota mediates activation of the NF-κB pathway, which then stimulates the secrete a large amount of proinflammatory cytokines. The elevated IL-6/IFN-γ activates the JAK2/STAT3 pathway, which in turn secretes more proinflammatory cytokines, facilitates the self-perpetuation of proinflammatory microenvironment and promotes IBD progression. The data are presented as the mean ± SD. One-way ANOVA was used for statistical analysis