Fig. 6

Glutamine synthetase inhibition could erase ADSC-EXO therapeutic effect on hepatic fibrosis. A Schematic illustration of DEN/CCl₄-induced liver fibrosis model, ADSC-EXO treatment strategy and hepatic glutamine synthetase inhibition treated with MSO (10 mg/kg). B Liver/body weight ratio of vehicle (PBS), DEN/CCl₄ mice, DEN/CCl₄ + EXO mice, DEN/CCl₄ + EXO + MSO mice (n = 6/group). C Representative images of liver gross, H&E staining (scale bar, 50 μm), Sirius Red staining (scale bar, 100 μm) and IHC staining of α-SMA in each group mice liver sections. D Ishak score statistical of each group mice. E Quantitative statistics of Sirius Red staining by Image J software analysis (6 replicates). F Quantification statistic of α-SMA⁺ area% in α-SMA IHC slices by Image J software analysis (5 replicates). G Hepatic function serology markers AST and ALT level in mice serum. H Representative immunofluorescent staining of ALB (green) and Glul (Red) in each group paraffin-embedded liver sections with different treatments (scale bar, 200 μm). I Protein expression level of α-SMA and Glul in mice liver tissue was evaluated by western blot analysis. (Each lane represents one mouse, 3 replicates.) J Quantification statistic of (I). K Plasma ammonia level in each group mice. L Glutamate and glutamine concentration in liver tissue. M GSH concentration in liver tissue. All data are shown as the mean ± SEM, *p < 0.05, **p < 0.01, comparing with corresponding controls by unpaired t test between two groups. Aberrations: Glu, glutamate; Gln, glutamine; GSH, glutathione