Fig. 9

Microglial depletion ameliorated the activation of the NF-κB inflammatory pathway, hippocampal inflammation, complement activation, and synaptic elimination, and neuroinflammatory inhibition also rescued synaptic elimination. A, B Microglial depletion reduced the level of IL-1β (A) and TNF-α (B) in the hippocampus (n = 4 per group). C Microglial depletion decreased the expression of C1qa in the hippocampus (n = 4 per group). D Microglial depletion decreased the expression of CD68 in the hippocampus (n = 4 per group). E Immunoblotting band of C1qa, CD68, Phospho-NF-κB p65, and β-actin. F Microglial depletion reduced the expression of Phospho-NF-κB p65 in the hippocampus (n = 4 per group). G, H Microglial depletion increased the expression of SYP in the hippocampus (n = 4 per group). Microglial depletion rescued synaptic loss in the hippocampus. I, J Microglial depletion increased the expression of SYN1 (I) and PSD95 (J) in the hippocampus (n = 4 per group). K The schedule of the third experiment. Intraperitoneal injection of meloxicam was administered three times: at the time of sevoflurane exposure, at the time of anesthesia end, and 1 h after anesthesia end. L Neuroinflammatory inhibition also reduced complement and rescued synaptic elimination. M Neuroinflammatory inhibition decreased the level of IL-1β in the hippocampus (n = 4 per group). N Neuroinflammatory inhibition decreased C1qa expression in the hippocampus (n = 3 per group). O, P Neuroinflammatory inhibition increased SYN1 (O) and PSD95 (P) expression in the hippocampus (n = 3 per group). Q Suppression of neuroinflammation inhibiting complement-mediated synaptic loss (n = 4 per group). Scale bar = 50 μm. Data was shown as Mean ± SD, with *P < 0.05 or *P < 0.001; Sevo-NS group vs. Sevo-Meloxicam group. Arrows represent colocalization