Skip to main content
Fig. 4 | Journal of Translational Medicine

Fig. 4

From: An Fgr kinase inhibitor attenuates sepsis-associated encephalopathy by ameliorating mitochondrial dysfunction, oxidative stress, and neuroinflammation via the SIRT1/PGC-1α signaling pathway

Fig. 4

Fgr inhibitor treatment suppressed ROS generation and mitochondrial injury in the hippocampus of septic mice. A Representative TEM image of mitochondria in the hippocampus (scale bar, 2 μm or 500 nm). B, C Statistical analysis of mitochondrial density and length (n = 5 mice, mean ± SEM, one-way ANOVA with Bonferroni post hoc test, *p < 0.05, **p < 0.01). D Representative DHE staining fluorescence of ROS in the hippocampus (scale bar, 200 μm or 100 μm). E Relative level of ROS (normalized to the sham group) (n = 5 mice, 3–4 slices per mouse, mean ± SEM, one-way ANOVA with Bonferroni post hoc test, **p < 0.01, ***p < 0.001). F ATP content in the hippocampus of the indicated groups (n = 5 or 7 mice, mean ± SEM, one-way ANOVA with Bonferroni post hoc test, **p < 0.01, ***p < 0.001). GK Mitochondrial respiratory chain complex (I, II, III, IV, and V) enzyme activity in the hippocampus (n = 3 mice, mean ± SEM, one-way ANOVA with Bonferroni post hoc test, *p < 0.05, **p < 0.01, ***p < 0.001)

Back to article page