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机构地区:[1]滨州医学院基础学院,山东烟台264003 [2]滨州医学院临床学院,山东滨州256603
出 处:《中国病理生理杂志》2011年第12期2328-2332,共5页Chinese Journal of Pathophysiology
基 金:山东省高等学校科技计划(No.J09LF64);2009年山东省高等学校优秀青年教师国内访问学者资助项目(No.2009GN003)
摘 要:目的:研究人参皂苷Rg1对大鼠脑缺血再灌注损伤的影响及其作用的机制。方法:采用大鼠右侧大脑中动脉阻塞(MCAO)2 h、再灌注24 h模型,造模前,人参皂甙Rg1防治组分别静脉注射人参皂苷Rg1 10、20及40 mg/kg,1次/d,连续7 d。分别以Longa's法评定神经功能、尼氏染色观察海马椎体细胞存活数,并检测脑组织中内一氧化氮(NO)含量及一氧化氮合酶(NOS)、诱导型一氧化氮合酶(iNOS)活性,Western blotting检测脑组织中神经元型一氧化氮合酶(nNOS)和iNOS蛋白表达。结果:与模型组比较,人参皂苷Rg1 20及40 mg/kg组能明显改善大鼠MCAO后神经功能症状,增加海马椎体细胞存活数(P<0.05,P<0.01),使脑组织NOS和iNOS活性降低,NO生成减少(P<0.05,P<0.01),iNOS及nNOS表达不同程度降低(P<0.05,P<0.01)。结论:人参皂苷Rg1能减轻大鼠脑缺血再灌注损伤,其机制可能与抑制NOS表达而使NO含量降低有关。AIM: To observe the neuroprotective effects of ginsenoside Rg1 on focal cerebral ischemia reperfusion(I/R) injury in rats.METHODS: SD rats were applied to right middle cerebral artery occlusion(MCAO) for 2 h followed by 24 h of reperfusion.The rats were randomly divided into sham-operation group,I/R group and ginsenoside Rg1 pretreatment groups.The rats in ginsenoside Rg1 pretreatment groups were pretreated with ginsenoside Rg1 at doses of 10,20 or 40 mg/kg once a day for 7 days and then subject to MCAO.The neurological deficit score was measured by Longa's method.The neurons were observed with Nissel staining.The nitric oxide(NO) content,the activity of nitric oxide synthase(NOS) and inducible NOS(iNOS) in the brain tissues were determined.The expression of neuronal NOS(nNOS) and iNOS was detected by Western blotting.RESULTS: Compared with sham-operation group,ginsenoside Rg1 significantly reduced the neurological deficit score and increased the neuron number in the hippocampus.The activity of NOS and iNOS,and NO content were decreased.Ginsenoside Rg1 also down-regulated the expression of nNOS and iNOS.CONCLUSION: Ginsenoside Rg1 has protective effect on the brain during cerebral I/R injury in rats.The mechanism may be related to reducing the content of NO and the activiy of NOS dose-dependently.
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