Fig. 9

As innate immune cells in the CNS, microglia are activated after SAH in vivo and in vitro. Microglia then initiate an inflammatory cascade to aggravate neuronal damage, which is an important cause of EBI. A neurosteroid, DHEA, exerts an anti-inflammatory effect after Hb exposure by initiating the TrkA/Akt signalling pathway and inducing the expression of the H3K27me3 demethylase, Jmjd3. Jmjd3 then negatively regulates proinflammatory genes and modulates the proinflammatory/anti-inflammatory switch, possibly through its downstream transcription factors