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机构地区:[1]中国药科大学分析测试中心电镜室 [2]中国药科大学生命科学与技术学院
出 处:《中国临床药理学与治疗学》2009年第4期391-396,共6页Chinese Journal of Clinical Pharmacology and Therapeutics
摘 要:目的:观察丹参酮ⅡA纳米制剂对大鼠全脑缺血再灌注损伤的保护作用。方法:采用三动脉夹闭法制备大鼠全脑缺血再灌注损伤模型,以丹参酮ⅡA纳米制剂灌胃给药,观察丹参酮ⅡA纳米制剂对脑组织的丙二醛(MDA)含量、超氧化物歧化酶(SOD)活力和脑组织Na+-K+-ATPase活性水平的影响。做脑组织病理切片检查和透射电镜观察。结果:丹参酮ⅡA纳米制剂(25 mg/kg)能使脑组织MDA含量下降(P<0.01),SOD活性明显升高(P<0.05),Na+-K+-ATP活性显著上升(P<0.01),病理切片和透射电镜观察显示丹参酮ⅡA纳米制剂能在不同的水平上抑制细胞和线粒体的损伤。结论:丹参酮ⅡA纳米制剂对全脑缺血再灌注损伤具有很好的保护作用。AIM: To investigate the protection effect of preparation of nanometer Tanshinone Ⅱ A against brain injury in rats undergone global cerebral ischemia reperfusion. METHODS: The rats were intragastrically administrated with the preparation of nanometer Tanshinone Ⅱ A, then the global cerebral ischemia-reperfusion model of rat was made by clipping and Measing three arteries. The content of MDA and the activity of SOD and Na^+ -K^+ -ATPase in homogenate of the cerebral tissues were measured. The sections of pathology and uhrastmcture of mitochondrion in cortex had been observed. RESULTS: Tanshinone Ⅱ A ( 25 mg/kg) could obviously decrease the content of MDA (P 〈0.01) and increase the activity of SOD(P 〈 0.05) and Na^+-K^+ -ATPase( P 〈 0.05) in rats brain tissue. The observation of pathology and ultrastructure showed that the injury of cell and mitochondrion had been restrained in these of rat brain. CONCLUSION: Preparation of nanometer Tanshinone ⅡA has protective effect against global cerebra injury caused by global cerebral ischemia-reperfusion injury in rats.
关 键 词:丹参酮ⅡA纳米制剂 全脑缺血再灌注 自由基 NA^+-K^+-ATP酶 细胞超微形态
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