【摘要】 目的研究知母皂苷化合物对脑缺血再灌注大鼠的保护作用及其机制。方法采用播线法制备脑缺血再灌注模型,观察大鼠的神经症状、脑梗塞范围、血细胞计数;测定超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)、总一氧化氮合酶(T NOS)、诱导型一氧化氮合酶(i NOS)活性以及丙二醛(MDA)、一氧化氮(NO)含量。结果知母皂苷化合物20、40mg/kg组能明显减轻脑缺血再灌注大鼠的神经症状、减小脑梗塞范围,降低全血中的白细胞计数及中性粒细胞计数,能明显降低脑组织中的MPO活性、提高SOD活性、减少MDA含量、减少NO含量、降低T NOS、i NOS活性。结论知母皂苷化合物通过减轻自由基损伤、炎症反应以及NO的毒性作用,从而对脑缺血再灌注大鼠具有一定的保护作用。更多还原

【Abstract】 Objective To investigate the protective effects of a saponin compound from Anemarrhena asphodeloides (SCAA) on the rat undergone cerebral ischemia/reperfusion and to study the mechanism of the effects. Method The rat model of cerebral ischemia/reperfusion was induced by the thread insertion method, in which the neurological symptoms, area of cerebral infarction, and blood cell count were observed, and the activities of SOD, MPO and NOS, and the levels of MDA and NO were detected. Results It was found that when being used at doses of 20 mg/kg and 40 mg/kg, respectively, in the model rats, SCAA showed marked effects of relieving the neurological symptoms; reducing the area of cerebral infarction; decreasing the white blood cell count and neutrophil blood count in the whole blood; reducing the activities of MPO, T-NOS, and i-NOS; increasing the activity of SOD; and decreasing the levels of MDA and NO. Conclusion The mechanism of SCAA in protecting the rat from cerebral damage due to ischemia/reperfusion is its reducing the intensities of the injury caused by free radicals, inflammatory reactions, and of the NO toxic effects.更多还原