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作 者:赵学萍 吴苗苗[1] 吴志刚[1] 董晓华[1] ZHAO Xue-ping;WU Miao-miao;WU Zhi-gang;DONG Xiao-hua(Hebei North University,Zhangjiakou 075000,China)
出 处:《中成药》2018年第10期2131-2134,共4页Chinese Traditional Patent Medicine
基 金:河北省教育厅重点课题(ZD2014065);张家口市科技局资助课题(0291098D);河北北方学院自然科学研究计划项目(2009033)
摘 要:目的考察丹酚酸B、三七皂苷R_1不同配伍比例对脑缺血再灌注损伤大鼠的影响。方法线栓法制备大鼠右侧大脑中动脉栓塞模型。大鼠随机分为假手术组、模型组、丹酚酸B组(120 mg/kg)、三七皂苷R_1组(120 mg/kg)、配伍组[丹酚酸B+三七皂苷R_1,60 mg/kg+60 mg/kg (1∶1)、40 mg/kg+80 mg/kg (1∶2)、80 mg/kg+40 mg/kg(2∶1)],各组给药14 d。然后,计算神经功能缺损评分,评价学习记忆能力,测定海马SOD活性、MDA含有量。结果与模型组比较,给药组神经功能缺损评分均有所降低,学习记忆能力均有所改善,以配伍组(1∶2)作用最强;除丹酚酸B组外,给药组SOD活性显著升高,MDA含有量显著降低(P <0. 05,P <0. 01),以配伍组(1∶2)作用最强。结论丹酚酸B与三七皂苷R_1的最佳配伍比例为1∶2,此时对脑缺血再灌注损伤大鼠的神经保护作用最强。AIM To investigate the effects of different compatibility proportions of salvianolic acid B and noto- ginsenoside R1 on cerebral ischemia-repeffusion injury in rats. METHODS The rat model for right middle cere- bral artery embolism was prepared by thread embolism method. The rats randomly divided into sham operation group, model group, salvianolic acid B group (120 mg/kg), notoginsenoside R1 group (120 mg/kg) and compati- bility groups [ salvianolic acid B + notoginsenoside R1, 60 mg/kg + 60 mg/kg ( 1 : 1 ), 40 mg/kg + 80 mg/kg (1 : 2), 80 mg/kg + 40 mg/kg (2 : 1 ) ] were all given administration for 14 d, then neural function defect score was calculated, learning and memory abilities were evaluated, hippocampus SOD activity and MDA content were determined. RESULTS Compared with the model group, neural function defect scolds were decreased in the ad- ministration groups with improved learning and memory abilities, especially for those in the compatibility group (1 : 2). Except for the salvianolic acid B group, the administration groups demonstrated significantly increased SOD activities and decreased MDA contents (P 〈 0.05, P 〈 0.01 ) , especially for those in the compatibility group (1 : 2 ). CONCLUSION The optimal compatibility proportion of salvianolic acid B to notoginsenoside R1 is 1 : 2, which exerts the strongest neuroprotective effects on cerebral ischemia-repeffusion injury in rats.
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