Peroxisome proliferator-activated receptor-γ agonist rosiglitazone reduces secondary damage in experimental spinal cord injury

Objective To investigate the neuroprotective effects of rosiglitazone in a rat traumatic spinal cord injury (SCI) model. Methods Adult Sprague–Dawley rats ( n = 12/group) underwent laminectomy (sham), SCI, SCI and rosiglitazone treatment (2 mg/kg twice daily for 7 days), or SCI and saline injection (vehicle). SCI was induced via dural application of an aneurysm clip. Spinal cord apoptosis and levels of tumour necrosis factor-α (TNFα), interleukin (IL)-1β, myeloperoxidase (MPO) and the apoptosis-associated proteins B-cell leukaemia/lymphoma 2 (Bcl-2) and Bcl-2 associated X protein (Bax) were examined 24 h after SCI. Locomotor function was evaluated 3, 7, 10, 14 and 21 days after SCI. Results At 24 h after SCI, apoptosis and TNFα, IL-1β and MPO concentrations were significantly lower in the rosiglitazone group than in the vehicle and SCI groups. SCI resulted in an increase in Bax and a decrease in Bcl-2, which was reversed by rosiglitazone treatment. Rats in the rosiglitazone group had significantly better functional recovery than those in the vehicle and SCI groups. Conclusion Rosiglitazone significantly improved functional recovery, probably via attenuation of the local inflammatory reaction and reduced apoptosis.