This study aims to reveal the role of necroptosis after SAH, and explore whether the disruption of the blood-brain barrier (BBB) and RIP3-mediated necroptosis following SAH in a rat SAH model are altered by necrostatin-1 via its selective inhibition of receptor-interacting protein kinase 1 (RIP1).
Our results showed that the expression levels of necroptosis-related proteins including RIP1, RIP3 and MLKL in the basal cortex all increased at 3 hours after SAH (<i>P</i><0.05) and peaked at 48 hours after SAH (<i>P</i><0.05).
Additionally, we verified the presence of RIP3-mediated necroptosis in an in vitro SAH model of primary cultured neurons treated with conditioned medium from primary microglia activated by oxygen hemoglobin (OxyHb).