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作 者:韩玉霞[1] 魏欣冰[1] 李霞[2] 丁燕[1] 辛华[2] 丁华[1]
机构地区:[1]山东大学医学院药理学研究所,济南250012 [2]山东大学医学院细胞生物学研究所,济南250012
出 处:《山东大学学报(医学版)》2008年第5期449-452,共4页Journal of Shandong University:Health Sciences
基 金:山东省自然科学基金资助课题(Y2006C41)
摘 要:目的探讨绞股蓝总皂苷(gypenosides,GP)对大鼠侧脑室注射谷氨酸(glutamate,Glu)引起的海马组织氧化损伤的保护作用。方法将大鼠随机分为假手术组、Glu损伤组、GP低(200 mg/kg)、中(400 mg/kg)、高(800 mg/kg)剂量组。GP组预先灌胃给药10 d。大鼠经侧脑室注射Glu后2 h取脑,测定各组大鼠海马组织匀浆中的丙二醛(MDA)含量、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性及产生羟自由基的能力;制备海马组织切片,观察各组形态学变化。结果Glu损伤组大鼠海马组织中MDA含量和羟自由基生成能力均高于假手术组(P<0.05),而SOD和GSH-Px活性降低(P<0.05);与Glu损伤组比较,GP组MDA含量和产生羟自由基的能力降低(P<0.01),SOD和GSH-PX活性明显增强(P<0.01);HE染色显示,GP组海马神经元变性及坏死较Glu损伤组明显减少。GP 400 mg/kg对Glu所致海马组织氧化损伤的保护作用最为明显。结论GP通过增强抗氧化酶活性,抑制羟自由基和脂质过氧化物生成而减轻Glu介导的氧化性神经损伤,发挥神经保护作用。Objective To investigate the protective effects of gypenosides(GP) against glutamate-induced oxidative injury to the hippocampus of rats. Methods 60 Wistar rats were randomly divided into 5 groups: the sham-operation group, the glutamateinduced injury group, the GP low (200 mg/kg), medium(400 mg/kg) and high (800 mg/kg) dose groups. Intra-gastric administration of GP was used for 10 d. 2 h after injection with glutamate through the lateral ventricle, the homogenate of the hippocampus was collected and the MDA, SOD, GSH-Px activity and the hydroxyl radical generation capacity were determined. Results: The MDA concentration and hydroxyl radical generation capacity were significantly increased( P 〈 0.05), however activities of SOD and GSH-Px were significantly decreased ( P 〈 0.01)in the glutamate-induced injury group compared with the sham-operation group. Also, the MDA concentration and hydroxyl radical generation capacity were significantly decreased in the GP groups compared with the glutamate-induced injury group ( P 〈 0.01 ), and activities of SOD and GSH-Px were significantly increased (P 〈 0.01) by GP treatments, and 400 mg/kg GP had the most effective action. Conclusion The protective effects of GP against Glu-mediated nerve injury may be mediated by increasing the activity of antioxidant enzymes and inhibiting the hydroxyl radical production.
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