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).
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).
The present study aimed to investigate the RIPK3-mediated necroptosis and the effects of the RIPK3 selective inhibitor GSK'872 in early brain injury following SAH.
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).