罗格列酮对大鼠脑缺血/再灌注损伤的保护作用

目的探讨罗格列酮对局灶性脑缺血/再灌注损伤的保护作用及其机制。方法线栓法制备大鼠大脑中动脉局灶性脑栓塞模型,缺血2h,再灌注24h。评价神经功能状态,测定脑梗死体积;分光光度法测定组织丙二醛(MDA)和一氧化氮(NO)含量以及一氧化氮合酶(NOS)、超氧化物歧化酶(SOD)和髓过氧化物酶(MPO)活性。免疫组化法测定细胞间粘附分子-1(ICAM-1)表达,HE染色观察组织病理学改变。结果罗格列酮能降低缺血再灌注后脑梗死体积,改善神经功能状态,降低脑组织MDA、NO含量,升高SOD活性并降低NOS、MPO活性以及组织ICAM-1表达,同时能减轻脑组织病理学损害。结论罗格列酮对大鼠脑缺血/再灌注损伤具有明显保护作用,其机制与其清除氧自由基和抗炎有关。

Protective effect of rosiglitazone on cerebral ischemia/reperfusion injury in rats

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.