Fig. 4

Alleviation of sevoflurane-induced cognitive dysfunction by C1q inhibition through decreasing microglia-mediated synapse loss. A Representative Western blot bands of C1qa, Vglut2, and PSD95 in the hippocampus of control and sevoflurane-treated mice with IgG or anti-C1q (ANX005) treatment. B Compared to treatment with sevoflurane and IgG, ANX005 downregulated C1q expression and upregulated Vglut2 and PSD95 expression. n = 3. One-way ANOVA followed by a post hoc Tukey’s test. C Representative confocal images of Vglut2 (green) and PSD95 (red) in the four groups. Scale bars = 5 μm. D Quantification analysis showed that ANX005 treatment increased the density of Vglut2⁺ puncta, PSD95⁺ puncta, and synapses compared to treatment with sevoflurane and IgG. n = 6. One-way ANOVA followed by a post hoc Tukey’s test. E Representative Golgi-Cox staining images of dendrite spines in the four groups. Scale bars = 5 μm. F Quantification analysis showed that ANX005 treatment increased the spine density compared to treatment with sevoflurane and IgG. n = 6. One-way ANOVA followed by a post hoc Tukey’s test. G Representative confocal images of IBA1⁺ (red) containing PSD95⁺ puncta (green) in the four groups. Orthographic view and 3D rendering are shown. Scale bars = 5 μm. H Quantification analysis showed that ANX005 treatment decreased the engulfment index compared to treatment with sevoflurane and IgG. n = 20. One-way ANOVA followed by a post hoc Tukey’s test. I Tracking plots of mice in the Morris water maze test in the four groups. J ANX005 treatment reduced the escape latency compared to treatment with sevoflurane and IgG. n = 8. Two-way RM ANOVA followed by a post hoc Tukey’s test. (K) ANX005 treatment increased platform cross times and time spent in the target quadrant compared to treatment with sevoflurane and IgG. n = 8. One-way ANOVA followed by a post hoc Tukey’s test. Data are mean ± SEM. *P < 0.05, ** P < 0.01, *** P < 0.001