What question did this study set out to answer?

This research aims to evaluate the effect of pioglitazone on neuroinflammation and oxidative stress following subarachnoid hemorrhage.

May 15, 2026Open Access

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

Key Points

This research aims to evaluate the effect of pioglitazone on neuroinflammation and oxidative stress following subarachnoid hemorrhage.
Randomized trial with rodent model; groups included Sham, SAH, SAH+pioglitazone, and SAH+vehicle (8 per group).
SAH induced through autologous blood injection into the cisterna magna.
Pioglitazone (10 mg/kg) given 1 hour post-SAH; serum levels of IL-6, IL-1β, and MDA measured at 24 hours.
Pioglitazone significantly reduced levels of IL-6 and IL-1β (p<0.05).
Malondialdehyde levels were also decreased with pioglitazone treatment (p<0.05).
Histopathological analysis showed reduced neuronal injury in the hippocampus in the pioglitazone group.

Abstract

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.

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