莱菔硫烷对大鼠局灶性脑缺血再灌注损伤的保护作用及机制研究

目的 探讨莱菔硫烷对大鼠局灶性脑缺血再灌注损伤的保护作用及机制.方法 采用线栓法制备大鼠大脑中动脉阻断局灶性脑缺血模型,分别于MCAO后1h腹腔注射莱菔硫烷2.5mg/kg、5mg/kg、10mg/kg.于缺血2h再灌注24h时进行神经行为缺损评分,TTC染色评价脑梗死体积,测定脑组织中超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量.免疫荧光组织化学染色法检测黄核蛋白NQ01和脂质过氧化酶Prx6的表达.结果 莱菔硫烷给药组与对照组相比均能改善大鼠脑缺血再灌注后神经行为缺损评分,减少脑梗死体积.其中5mg/kg组能显著改善大鼠脑缺血再灌注后神经行为缺损评分,减少脑梗死体积,增强SOD活性,降低MDA含量.免疫荧光组织化学染色法提示NQ01和Prx6的表达明显增强.结论 莱菔硫烷对大鼠局灶性脑缺血再灌注损伤有神经保护作用,其机制可能与上调内源性抗氧化蛋白NQ01和Prx6的表达有关.

Neuroprotective effect and possible mechanisms of sulforaphane on focal cerebral ischemic-reperfusion injury in rats

Objective To explore the effects and possible mechanisms of sulforaphane on focal cerebral ischemia/reperfusion injury in rats.Methods Focal cerebral ischemia in rats was induced by 24h occlusion of the middle cerebral artery(MCAO).The administration doses of 2.5mg/kg,5mg/kg and 10mg/kg of SFN were provided at 1h after the onset of ischemia through intraperitoneal injection.The infarct area was measured by 2,3,5-triphenyltetrazolium chloride(TTC)staining.The neurological deficit score and brain edema were examined.The activities of antioxidase SOD and contents of MDA in ischemic brain tissue were analyzed.The expression of NQO1 and Prdx6 were detected by immunofluorescence.Results All the sulforaphane groups may reduce the neurological deficit score,infarct size and brain edema,especially the 5mg/kg sulforaphane group showed significant reduced neurological deficit score,infarct size and brain edema.Striking increase in activities of SOD and significant decrease in contents of MDA in rats were also observed after 24h of MCAO.The expression of NQO1 and Prdx6 was remarkably increased by sulforaphane.Conclusion Sulforaphane has valid protective effect on cerebral ischemia/reperfusion injury.Sulforaphane plays satisfactory neuroprotective effect after focal cerebral ischemia-reperfusion injury which may be associated with up-regulating the expression of NQO1 and Prx6.