NFKB1 and subarachnoid hemorrhage: AE can impede apoptosis by reducing the cysteine aspartate protease (Caspase-3) expression levels [25] and can treat subarachnoid hemorrhage (SAH) by modulating the NF-κB and cyclic adenosine phosphate/protein kinase A/responsive element binding protein pathways, thereby inhibiting hemorrhage-induced inflammatory cytokines and nerve cell apoptosis [26].