浅析葛根素对大鼠局灶性缺血脑组织内海马神经元型一氧化氮合酶表.docVIP

浅析葛根素对大鼠局灶性缺血脑组织内海马神经元型一氧化氮合酶表 　【摘要】 目的观察葛根素对大鼠局灶性脑缺血海马神经元神经型一氧化氮合酶(nNOS)表达的影响。方法局灶性脑缺血模型由线栓法阻塞大鼠大脑中动脉制成，葛根素腹腔注射干预治疗，采用氯化三苯基四氮唑染色方法测定脑梗死体积，免疫组织化学方法测定大鼠脑缺血后不同时间点前后海马区nNOS阳性神经元表达的变化。结果2h和12h干预组脑梗死体积明显小于对照组(Plt;0.05)，24h干预组与对照组比较无统计学差异(Pgt;0.05)。缺血2h组海马nNOS阳性细胞开始增加，12h组最高，24h组较前有所下降;干预组大鼠海马nNOS阳性细胞数与对照组比较降低明显，有统计学差异(Plt;0.01)。结论nNOS参与早期脑缺血损伤，葛根素通过抑制nNOS表达对大鼠脑神经元损伤起保护作用。 【关键词】 大鼠;葛根素;脑缺血损伤;神经型一氧化氮合酶;海马 　 ABSTRACT: ObjectiveTo observe the effect of Puerarin on the expression of neuronal nitric oxide synthase (nNOS) in hippocampal neurons after focal cerebral ischemia in rats.MethodsThe model of focal cerebral ischemia was established by achieving middle cerebral artery occlusion in rats with thread. The rats were divided into different ischemia time groups, including 2 hour, 12 hour and 24 hour ischemic models and the control. Puerarin was injected intraperitoneally into the models. The volume of cerebral infarction was determined by tripheye tetrazolium chloride (TTC) staining. The expression of nNOS-positive neurons in the hippocampus was determined by immunohistochemistry.ResultsThe cerebral infarction volume in 2-hour and 12-hour Puerarin intervention groups was significantly smaller than that of the control (Plt;0.05), but there was no difference between the 24 hour ischemic model and the control (Pgt;0.05). The number of nNOS-positive cells in the hippocampus started to increase in the 2-hour ischemic rats, and reached the peak in the 12-hour ischemic rats. The nNOS-positive cells in the Puerarin-therapy rats decreased significantly (Plt;0.01) compared with those in the controls.ConclusionnNOS is involved in the early ischemic brain injury. Puerarin may protect the brain neurons from ischemic injury by inhibiting the expression of nNOS in the neurons. 　　KEY WORDS: rat; Puerarin; cerebral ischemic injury; nitric oxide synthase; hippocampus 　　神经型一氧化氮合酶(neuronal nitric oxide synthase, nNOS)主要存在于神经细胞，生理状态下活性很低，一旦被激活，则可持续产生大量一氧化氮(nitric oxide, NO)，参与脑缺