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

J Int Med Res

Department of Orthopaedic Surgery, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

Published: February 2013

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.

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http://dx.doi.org/10.1177/0300060513476601DOI Listing

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