Fig. 3
Disruption of myeloid-specific PTEN prevents glycogen synthase kinase-3β (GSK3β) and activates the NICD/NRF2 pathway in AILI. PTENFL/FL and PTENM−KO mice were subjected to APAP (400 mg/kg) challenge for 24 h. A Western-assisted analysis and relative density ratio of p-Akt, Akt, p-GSK3β, GSK3β, NICD, and NRF2 with or without APAP-challenged PTENFL/FL livers (n = 6 samples/group). B Western-blot analysis and relative density ratio of p-Akt, Akt, p-GSK3β, and GSK3β in the PTENFL/FL and PTENM−KO mice liver after APAP challenge (n = 6 samples/group). C Immunofluorescence staining of p-GSK3β and CD68 in AILI liver tissue (n = 6 mice/group). Scale bars, 100 μm. D Western-blot analysis and relative density ratio of p-PS1, PS1, and NICD in the PTENFL/FL and PTENM−KO mice liver after APAP-treated (n = 6 samples/group). E Western-blot analysis and relative density ratio of NRF2 in the PTENFL/FL and PTENM−KO mice livers after APAP-treated. Data representative of three experiments. F Quantitative RT-PCR analysis of Nqo1, Gclc, and Gclm mRNA levels in PTENFL/FL and PTENM−KO mouse livers with or without APAP-treated (n = 6 samples/group). G The liver macrophages were isolated from APAP-treated livers, and then these cells were cultured for 2 h at 37℃. Detection of ROS generation by Carboxy-H2DFFDA in LPS-stimulated macrophages from the PTENFL/FL and PTENM−KO mice. Quantification of ROS-producing Macrophages (green) (n = 6 mice/group). Scale bars, 100 μm. All data represent the mean ± SD. **p < 0.01, ****p < 0.0001