Fig. 6

tPBM diminished PI-induced neuroinflammation in the mouse hippocampus. A Activation of microglia and astrocyte in CA1, CA3 and hilus was confirmed 7 days after PBM in PI-induced mouse excitotoxicity. IHC-stained CD11b and GFAP show the reactive form of microglia and astrocytes in each hippocampus region. Conditions were untreated sham, PI only and PI + tPBM with 825 nm groups. The stained images show that the number of reactive astrocytes and microglia was significantly lower in the 825 nm treated group compared to the PI only group. The scale bars indicate 100 μm. B, C The numbers of GFAP-immunostained reactive astrocytes and CD11b-immunostained reactive microglia in hippocampal CA1, CA3, and hilus were analyzed. These analyses revealed that tPBM significantly reduced the number of reactive glial cells in the hippocampus. Data are expressed as the mean ± SEM; *p < 0.05, ***p < 0.001 relative to sham, ^#p < 0.05, ^##p < 0.01, ^###p < 0.001, ^####p < 0.0001 relative to PI (ANOVA with the Bonferroni test). D, E GFAP, IBA1 and COX2 protein levels of homogenized hippocampus tissues were determined by western blotting. β-actin was used as a loading control. Data analysis was performed using ImageJ software by measuring the integrated band densities following background subtraction. Full-length blots/gels are presented in Additional file 1: Fig. S3. Data are expressed as the mean ± SEM; ***p < 0.001 relative to PI (Mann–Whitney U test), ****p < 0.0001 relative to PI (Student’s t-test). F Quantitative analyses of the prostaglandin E₂ in homogenized hippocampus tissues in the PI and PI + tPBM groups. Data are expressed as the mean ± SEM; **p < 0.01 relative to PI (Student’s t-test)