Pioglitazone mitigates early brain injury by suppressing neuroinflammation and oxidative stress after subarachnoid hemorrhage: a rodent model study

OBJECTIVE: Subarachnoid haemorrhage (SAH) is a devastating neurovascular emergency where outcomes are largely driven by early brain injury (EBI). Neuroinflammation and oxidative stress are central to EBI pathogenesis. This study experimentally evaluated whether pioglitazone attenuates inflammatory and oxidative responses in the early phase after SAH. MATERIALS AND METHODS: = 8/group): Sham, SAH, SAH+pioglitazone (PIO), and SAH+vehicle (VEH). SAH was induced by autologous blood injection into the cisterna magna. Pioglitazone (10 mg/kg, intraperitoneally) was administered 1 h post-SAH. Serum interleukin-6 (IL-6), interleukin-1β (IL-1β), and malondialdehyde (MDA) levels were quantified by Enzyme-Linked Immunosorbent Assay (ELISA) at 24 h. Hippocampal neuronal injury was assessed using semi-quantitative histopathological analysis of haematoxylin-eosin-stained sections. Acute-phase biochemical and histopathological effects were evaluated; long-term functional outcomes were not assessed. RESULTS: < 0.05). CONCLUSION: peroxisome proliferator-activated receptor-γ (PPAR-γ) activation.