Fig 1: Knockdown of RIP3 expression inhibits inflammatory signaling pathways in vitro. A–C ELISA assay detected the effect of RIP3 knockdown plasmid and RIP3 inhibitor GSK872 on the secretion of inflammatory factors IL-16, IL-17 and IFN-? after TNF-a (10 ng/ml, 12 h) treatment. D Western blot detected the effect of shRIP3 knockdown plasmid and RIP3 inhibitor GSK872 on the expression of key molecules in the TLR4/MyD88/NF-?B signaling pathway. The semi-quantitative analysis of western blotting via Image J software (right panel). E After cultured with TNF-a (10 ng/ml, 12 h), shRIP3 plasmid, or RIP3 inhibitor GSK872, cells were incubated with DAFH-DA probe and the results were observed under fluorescence microscope with a 10 × objective. Scale bar: 200 µm. The semi-quantitative analysis of immunofluoresence via Image J software (right panel)
Fig 2: Nec-1 treatment could relieve DSS-induced intestinal inflammation in vivo. A–C ELISA detected the secretion of IL-17, IFN-? and IL-10 cytokines in mouse colon tissue. D–E Flow cytometry analyzed the proportion of CD4+ Foxp3+ T cells in CD4+ T cells of mouse spleen
Fig 3: Comparison of BTNL8 expression with postoperative serum inflammatory factors. Comparison of BTNL8 expression with postoperative serum (A) IL-17 levels; (B) IL-23; (C) IL-10 levels. ** vs. p < 0.01; *** vs. p < 0.001; **** vs. p < 0.0001.
Supplier Page from Abcam for Human IL-17 ELISA Kit