Fig. 5: AKT is required for the regulation of MST1/NRF2 in myeloid TSC1-deficient livers in response to I/R stress. | Cell Death & Disease

Fig. 5: AKT is required for the regulation of MST1/NRF2 in myeloid TSC1-deficient livers in response to I/R stress.

From: Loss of macrophage TSC1 exacerbates sterile inflammatory liver injury through inhibiting the AKT/MST1/NRF2 signaling pathway

Fig. 5

Bone marrow-derived macrophages (BMMs) from TSC1M-KO mice were transfected with lentivirus expressing AKT (Lv-AKT) or GFP control (Lv-GFP) and adoptively transferred into TSC1M-KO mice. A Representative H&E and TUNEL staining of liver sections (n = 4–6 mice/group), Scale bars = 250 μm (H&E), Scale bars = 200 μm (TUNEL). B Liver damage, evaluated by Suzuki’s score. ***p < 0.001. C The number of apoptotic cells per field at 400× magnification. The results are representative of 4–6 mice/group. ***p < 0.001. D The serum ALT levels from the indicated groups. ***p < 0.001. E Representative immunohistochemistry staining and quantification of CD11b+ macrophages and Ly6G+ neutrophils in liver sections (n = 4–6 mice/group), Scale bars = 150 μm. **p < 0.01, ***p < 0.001. F Western blot analysis of p-AKT, p-MST1, MST1, NRF2, and TLR4. β-actin served as an internal control. Data are representative of three experiments. G Quantitative RT-PCR-assisted detection of TNF-α, IL-1β, IL-6 and TGF-β expression. Mean ± SD (n = 4–6 samples/group). **p < 0.01.

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