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目的:研究氧化槐定碱(Oxysophoridine,OSR)对小鼠脑组织急性缺血的保护作用。方法:ICR小鼠50只随机分为5组:对照组;OSR(62.51,25,250 mg/kg)组;尼莫地平(20mg/kg)组。各实验组分别灌胃7d,1次/d;对照组给予相同容积的生理盐水。末次给药后1小时,采用快速断头法制备小鼠急性全脑缺血模型。观察小鼠的喘息次数和喘息维持时间;取小鼠脑组织测定丙二醛(MDA)的含量和超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、乳酸脱氢酶(LDH)、肌酸激酶(CK)以及一氧化氮合酶(NOS)的活性。结果:与对照组比较,OSR(125、250mg/kg)组和尼莫地平(20mg/kg)组小鼠断头后喘息次数明显增加,喘息维持时间显著延长;与对照组比较,OSR(62.51、25、250mg/kg)组和尼莫地平(20mg/kg)组小鼠脑组织MDA含量明显降低;与对照组比较,OSR(1252、50mg/kg)组和尼莫地平(20mg/kg)组小鼠脑组织SOD、GSH-Px活性显著增高;与对照组比较,OSR(125、250mg/kg)组和尼莫地平(20mg/kg)组小鼠脑组织LDH、CK活性明显增高;与对照组比较,OSR(1252、50mg/kg)组和尼莫地平(20mg/kg)组小鼠脑组织NOS活性显著降低。结论:氧化槐定碱对小鼠急性脑缺血损伤有明显的保护作用,其作用机制可能与其抗氧化作用有关。
Objective: To study the protective effect of Oxysophoridine (OSR) on acute cerebral ischemia in mice. Methods: 50 ICR mice were randomly divided into 5 groups: control group; OSR (62.51,25,250 mg / kg) group; nimodipine (20 mg / kg) group. Each experimental group were administered 7d, 1 / d; control group were given the same volume of saline. One hour after the last administration, a mouse model of acute global cerebral ischemia was prepared by rapid decapitation. The numbers of wheezing and wheezing in mice were observed. The content of malondialdehyde (MDA) and the content of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), lactate Dehydrogenase (LDH), creatine kinase (CK) and nitric oxide synthase (NOS) activity. Results: Compared with the control group, OSR (125,250mg / kg) and nimodipine (20mg / kg) groups significantly increased wheezing and prolonged wheeze maintenance after OSA. Compared with the control group, OSR (62.51 , 25,250 mg / kg group and nimodipine (20 mg / kg) group were significantly lower than those of the control group. Compared with the control group, the levels of MDA in the OSR group (1252,50mg / kg) and nimodipine Compared with the control group, the activity of LDH and CK in the brain tissue of OSR (125,250mg / kg) group and nimodipine (20mg / kg) group were significantly increased, and the activity of SOD, GSH- Compared with control group, the activity of NOS in brain tissue of OSR (1252,50mg / kg) group and nimodipine (20mg / kg) group was significantly decreased. CONCLUSION: Oxalipine base has a significant protective effect on acute cerebral ischemia injury in mice, and its mechanism may be related to its antioxidative effect.