Fig. 5
NRF2 is vital for  inhibiting STING/TBK1 activation in macrophage PTEN‑mediated inflammatory in response to AILI. The PTENM−KO mice were injected via tail vein with Nrf2 siRNA (2 mg/kg) or non-specific (NS) control siRNA mixed with mannose-conjugated polymers at 24 h prior to APAP (400 mg/kg) treatment. A Western blot confirmed NRF2 expression with liver macrophages isolated for PTENM−KO mice. Data representative of three experiments. B Representative histological staining (H&E) of APAP-conditioning liver and Suzuki’s histological score (n = 6 samples/group). Scale bars, 200 μm. C Liver function was measured by serum ALT and AST levels (IU/L) (n = 6 samples/group). D Immunofluorescence staining of F4/80 macrophages in injured livers (n = 6 mice/group). Quantification of F4/80+ macrophages. Scale bars, 100 μm. E Immunohistochemistry staining of Ly6G neutrophils in injured livers (n = 6 mice/group). Quantification of Ly6G+ neutrophils. Scale bars, 100 μm. F Quantitative RT-PCR-assisted detection of Tnf-α, IL-1β, IL-6, Cxcl-1, and Mcp-1 mRNA levels in injured livers (n = 6 samples/group). G Western-assisted analysis and relative density ratio of p-STING, STING, p-TBK1, TBK1, p-IRF3, IRF3, p-P65, and P65 in injured livers. All data represent the mean ± SD. **p < 0.01, ***p < 0.001, ****p < 0.0001