Research ReportRosiglitazone attenuates early brain injury after experimental subarachnoid hemorrhage in rats

•Rosiglitazone improved neurological score and mortality in rats at 24 h after SAH.•We demonstrate that rosiglitazone protect against brain edema and BBB disruption at 24 h after SAH.•Significantly preservation of TUNEL assay, bcl-2 down-regulation and Bad translocation were showed after rosiglitazone usage.•Akt phosphorylation was activated by rosiglitazone in EBI after SAH.•We found that rosiglitazone showed neuroprotective and anti-apoptosis effect in EBI after SAH.

Early brain injury (EBI) plays a crucial role in the pathological progress of subarachnoid hemorrhage (SAH). This study was designed to determine whether rosiglitazone protects the brain against EBI in rats, and discuss the role of the anti-apoptotic mechanism mediated by Bcl-2 family proteins in this neuroprotection. 86 male Sprague-Dawley rats were divided into the sham group, the SAH+ vehicle group and the SAH+ rosiglitazone group. SAH was induced via an endovascular perforation technique and rosiglitazone (3 mg/kg) or vehicle was administered. Mortality, neurological scores, brain water content, Evans blue dye assay, TUNEL stain assay, Gelatin zymography, and western blot analysis were performed. Rosiglitazone significantly improved mortality, neurological scores, brain water content, blood brain barrier (BBB) and apoptosis compared with the vehicle group within 24 h after SAH. The TUNEL staining assay demonstrated that apoptosis was ameliorated. Cleaved Caspase-3 and MMP-9 expression was reduced, whereas Bcl-2 and p-Bad was markedly preserved by rosiglitazone. A significant elevation of p-Akt was detected after rosiglitazone treatment. Our study demonstrated that rosiglitazone plays a neuroprotective role in EBI after SAH via attenuation of BBB disruption, brain edema and apoptosis.