Fig. 10

Hyperoside mitigates microglial inflammatory activation and Müller cell gliosis. A Heatmap visualization of the representative genes implicated in microglial inflammatory activation and Müller cell gliosis revealed by RNA-seq analyses. B–E Real-time qPCR analysis validation of the genes associated with disease-associated microglial activation phenotypes (B) and microglial homeostasis (C), inflammatory responses (D) and Müller gliosis (E). Relative fold change was normalized against NLE. F Iba1 immunopositivity (in red) in the retina. DAPI (in blue) was counterstained to label the nuclei. White arrowheads indicated activated microglia in the outer retina. Scale bar, 50 μm. G GFAP immunopositivity (in red) in the retina. DAPI (in blue) was counterstained to label the nuclei. White arrowheads indicated aberrant GFAP expression indicative of reactive gliosis. Scale bar, 50 μm. Data were expressed as mean ± SEM (n = 6 per group). **Compared to NLE, P < 0.01; ***compared to NLE, P < 0.001; ^##compared to LE, P < 0.01; ^###compared to LE, P < 0.001. HYP the light-exposed mice treated with 50 mg/kg hyperoside, INL inner nuclear layer, IPL inner plexiform layer, LE the light-exposed mice treated with vehicle, NLE the vehicle-treated mice without light exposure, ONL outer nuclear layer, OPL outer plexiform layer