ABSTRACT
Aim To investigate the protective effect of rosiglitazone on cerebral ischemia/reperfusion injury inrats. Methods Transient focal cerebral ischemia injury model in rats was induced by occlusion of the right middle cerebral artery for 2 h, followed by 24 h reperfusion. The infarct volume and neurological deficit were determined by the method of TTC staining and the Longa′s score, and used to evaluate the effect of rosiglitazone on cerebral injury. The levels of malondialdehyde (MDA), nitric oxide (NO), activities of superoxide dismutase (SOD), myeloperoxidase (MPO) and nitric oxide synthase (NOS) in brain were measured by spectrophotometer. Immunohistochemistry was employed to assess the expression of intracellular adhesion molucule-1 (ICAM-1). The histopathological change was observed after HE staining. Results Pretreatment with rosiglitazone markedly reduced brain infarct volume and neurological deficit induced by transient ischemia, inhibited MPO activity, as well as expression of ICAM-1; it also decreased NO, MDA levels and NOS activity, increased SOD activity, and improved histopathological injury. Conclusion Rosiglitazone has a protective effect on cerebral ischemia/reperfusion injury through inhibiting inflammatory process and lipid peroxidation.