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补阳还五汤对体外培养的大鼠皮层神经元缺氧凋亡的影响
引用本文:曲宏达,佟丽,沈剑刚,陈育尧. 补阳还五汤对体外培养的大鼠皮层神经元缺氧凋亡的影响[J]. 南方医科大学学报, 2002, 22(1): 35-38
作者姓名:曲宏达  佟丽  沈剑刚  陈育尧
作者单位:第一军医大学中医系,广东,广州,510515;第一军医大学中医系,广东,广州,510515;第一军医大学中医系,广东,广州,510515;第一军医大学中医系,广东,广州,510515
基金项目:国家自然科学基金(39970900)
摘    要:目的探讨补阳还五汤对神经元缺氧凋亡的作用,以及对神经元缺氧过程氧自由基(OFR)、一氧化氮(NO)生成和bcl-2基因表达的影响。方法采用Daniel方法建立神经元缺氧凋亡模型,加入补阳还五汤药物血清,应用碘化丙啶(propidiumiodide,PI)染色法经流式细胞仪检测神经元凋亡率,分光光度法检测丙二醛(MDA)、NO浓度,免疫组化法检测bcl-2表达。结果补阳还五汤显著抑制缺氧导致的神经元凋亡,并减少神经元缺氧过程NO、OFR的生成,上调bcl-2基因的表达。结论补阳还五汤对神经元缺氧凋亡有抑制作用,其机制可能与其减少神经元缺氧过程NO、OFR生成,及上调bcl-2基因表达有关。

关 键 词:补阳还五汤  神经元  凋亡  bcl-2
文章编号:1000-2588(2002)01-0035-04
修稿时间:2001-06-04

Protective effect of Buyanghuanwu Tang on cultured rat cortical neurons against hypoxia-induced apoptosis
QUHong-da,TONGLi,SHENJian-gang,CHENYu-yao Departmentof TraditionalChineseMedicine,FirstMilitaryMedicalUniversity,Guangzhou,China. Protective effect of Buyanghuanwu Tang on cultured rat cortical neurons against hypoxia-induced apoptosis[J]. Journal of Southern Medical University, 2002, 22(1): 35-38
Authors:QUHong-da  TONGLi  SHENJian-gang  CHENYu-yao Departmentof TraditionalChineseMedicine  FirstMilitaryMedicalUniversity  Guangzhou  China
Affiliation:QUHong-da,TONGLi,SHENJian-gang,CHENYu-yao Departmentof TraditionalChineseMedicine,FirstMilitaryMedicalUniversity,Guangzhou510515,China
Abstract:Objective To investigatetheprotectiveeffectof BuyanghuanwuTang(BYHWT),a decoctionwith6herbal ingredients,on in vitro culturedratcorticalneuronsagainstapoptosisinducedby hypoxia,and studyitseffecton the productionof nitricoxide(NO) andoxygenfreeradicalsandBcl-2expressionin theneuronsduringhypoxia.Methods Modelsof hypoxia-inducedneuronapoptosiswere establishedand treatedwithsera containingBYHWT.Stainedby propidiumiodide,theneuronsunderwentapoptosisanalysisusingflowcytometry,andthelevelsof malonyldialdehyde(MDA) and NO weremeasuredwithspectrophotometer,withBcl-2expressionassayedby immunohistochemicalmethod withflowcytometry.Results In BYHWT-treatedneurons,apoptosisratesweresignificantlylowerthanthoseof theneurons subjectedto hypoxiaexclusively,andat thesametimeNO andMDAproductionwas remarkablyreduced.Bcl-2expression,however,wasup-regulated.Conclusion BYHWTcanprotectneuronsfromhypoxia-inducedapoptosis,themechanismof whichmay lie in the eliminationof NO and oxygenfreeradicalsproducedduringhypoxiaand up-regulationof Bcl-2expression.
Keywords:traditionalChinesemedicine  neuron  apotosis  bcl-2
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