葛根素对大鼠缺血性脑损伤的保护作用

［摘要］目的: 观察葛根素对大鼠全脑缺血/再灌注后神经元的保护作用，并探讨其可能的机制。方法： 采用四动脉结扎法建立大鼠全脑缺血模型, 缺血15 min后再灌注。将50只大鼠随机分为假手术组、缺血/再灌注组、给药组(细分为高、低剂量组)和对照组。给药方式为静脉注射。使用蛋白质印迹、焦油紫染色法及TUNEL法检测神经型一氧化氮合酶（neuronal NO synthase, nNOS)表达、nNOS活化水平及神经元细胞的存活情况。结果： 给药组大鼠海马CA1区细胞的存活数量较缺血/再灌注组明显增加(P<0.05)，TUNEL法检测结果与其一致；给药组nNOS(Ser847)磷酸化水平较缺血/再灌注组明显增强(P<0.05)，而其表达量没有明显变化。结论： 葛根素通过负向调节nNOS催化活性，减少NO生成，降低其神经毒性，对大鼠缺血性脑损伤有保护作用。

Puerarin protection against cerebral ischemia via inhibiting nNOS in rats

Objective： To evaluate the neuroprotection of puerarin against cerebral ischemia in SD rat models,and investigate the underlying mechanism.Methods： Fifty rats were randomly assigned into the following groups： sham-operated group,ischemia / reperfusion group,vehicle-treated group and drug-treated group.Transient brain ischemia（15 min） and reperfusion was induced by the four-vessel occlusion method（4-VO）.The expression and activity of neuronal NO synthase（nNOS） and the survival of neurons were performed by Western blotting,cresyl violet staining and TUNEL methods.Results： The drug-treated group showed high levels of neurons,which was consistent with the TUNEL results,and higher levels of nNOS phosphorylation,compared with the ischemia / reperfusion group（both P 0.05）.Conclusions： Puerarin could exert its neuroprotection from cerebral ischemia by increasing nNOS（Ser847） phosphorylation.