Fig. 11

Schematic representation of the effects of S100B and minocycline in this model. a Intravitrially injected S100B induced a pro-inflammatory response that included increased activation of microglia and release of inflammatory cytokines. Mass spectrometric proteome analysis indicates that S100B also caused mitochondrial dysfunction, which disrupts cellular metabolism and energy production. These two factors led to RGC degeneration and neurofilament loss. b Treatment with minocycline blocked microglia activation. Therefore, some RGCs were protected and the neurofilament remained largely intact. The apoptosis rate was also lowered. Neuronal damage was minimized, but not completely inhibited, since mitochondrial dysfunction and altered glycolysis have been induced despite minocycline treatment