Fig. 3. TIGAR-deficient reduces pro-inflammatory gene expression by inhibiting IKK-NF-κB signaling in macrophages.

a Western blot analysis of cell lysates from WT and Tigar KO BMDMs treated with LPS for the indicated times using the indicated antibodies (n = 3). b PMs isolated from WT and Tigar KO mice were treated with LPS for 3 h. Immunofluorescent staining of p65 (green) and DAPI (blue) (n = 3). Scale bars, 10 μm. c BMDMs isolated from WT and Tigar KO mice were treated with LPS for the indicated times. Western blot analysis of p65 subcellular distribution in the nucleus (n = 3). d RAW264.7 cells were transfected by Lenti-Con or Lenti-TIGAR for 72 h followed by LPS treatment for indicated time. Western blot analysis of cell lysates using the indicated antibodies (n = 3). e RAW264.7 cells were transfected by Lenti-Con or Lenti-TIGAR for 72 h followed by LPS treatment for indicated time. Western blot of p65 subcellular distribution in the nucleus from RAW264.7 cells treated with LPS for indicated times (n = 3). f RAW264.7 cells were transfected by Lenti-Con or Lenti-TIGAR for 72 h followed by LPS treatment with or without NF-κB pathway inhibitor BAY11-7082 for 12 h. mRNA levels of Tnf-α, Nos2, Ccl2, and Ccl8 were detected in the indicated groups (n = 3). Data are expressed as mean ± SEM. a–e Two-way ANOVA followed by the Bonferroni test. b Two-tailed Student t-test. f One-way ANOVA followed by the Bonferroni test. Source data are provided as a Source Data file.