Rosiglitazone attenuates inflammation and CA3 neuronal loss following traumatic brain injury in rats.

摘要: Rosiglitazone, a potent peroxisome proliferator-activated receptor (PPAR)-γ agonist, has been shown to confer neuroprotective effects in stroke and spinal cord injury, but its role the traumatic brain injury (TBI) is still controversial. Using controlled cortical impact model rats, current study was designed determine of rosiglitazone treatment (6 mg/kg at 5 min, 6 h 24 h post injury) upon inflammation histological outcome 21 d after TBI. In addition, inflammatory cytokine transcription, vestibulomotor behavior spatial memory function were determined earlier time points (24 h, 1-5 d, 14-20 d respectively). Compared with vehicle-treated group, suppressed production TNFα TBI, attenuated activation microglia/macrophages increased survival CA3 neurons had no effect on lesion volume Rosiglitazone-treated animals improved performance beam balance testing, there difference as by Morris water maze. summary, this indicates that first TBI limited anti-inflammatory rat injury. Further using an alternative dosage paradigm more sensitive behavioral testing may be warranted.