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黄芪预处理对缺血再灌注大鼠心肌细胞凋亡及相关基因的影响(英文) 被引量:15

Pre-treatment with radix astragali for myocardial cell apoptosis and its relative genes in rats with ischemic reperfusion
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摘要 背景:黄芪具有保护缺血再灌注细胞损伤的作用,黄芪预处理是否对缺血再灌注心肌细胞凋亡有保护作用?目的:探讨黄芪预处理对缺血再灌注大鼠心肌细胞凋亡及其相关基因的影响。设计:以Wistar实验大鼠为实验对象的随机分组对照。单位:承德医学院基础医学部及附属医院老年病科。材料:实验于2004-02/12在承德医学院基础医学研究所免疫组化实验室完成。选用雄性Wistar大鼠30只,将动物随机分为黄芪预处理组(黄芪组)、缺血再灌注组、假手术对照组(对照组),每组10只。方法:黄芪组术前给予腹腔内注射黄芪注射液,缺血再灌注组、对照组术前给予等量生理盐水注射。1周后制备缺血再灌注模型,术后即取缺血再灌注边缘区的心肌,对照组取相对应部位心肌。应用脱氧尿嘧啶缺口末端标记法测定心肌凋亡细胞指数的改变,应用免疫组化ABC法检测心肌细胞bcl-2(抑凋亡基因)及bax(促凋亡基因)基因的改变。主要观察指标:①各组凋亡细胞数。②bcl-2和bax基因表达情况。结果:①心肌凋亡细胞数:黄芪组低于缺血再灌注组[(14.06±9.97)%,(19.34±12.30)%,t=1.863,P<0.05]。②bcL-2基因表达:黄芪组与缺血再灌注组无明显差异[(9.14±4.46)%,(8.99±4.54)%,P>0.05]。③bax基因表达:黄芪组低于缺血再灌注组[(12.65±7.23)%,(18.12±7.92)%,t=2.096,P<0.05]。结论:黄芪预处理可使促凋亡基因bax的表达明显下调,从而使心肌细胞凋亡减少,保护缺血再灌注心肌细胞。 BACKGROUND: Radix astragali has the effect of protecting cells from damage in ischemic reperfusion, whether pre-treatment with radix astragali can protect myocardial cells from apoptosis in ischemic reperfusion *9芽 OBJECTIVE: To investigate the effect of pre-treatment with radix astragali on apoptosis and its relative genes in rats with ischemic myocardial reperfusion DESIGN: A randomized and controlled trial taking Wistar rats as experimental subjects. SETTING: The Basic Medical Department of Chengde Medical College and the Geriatric Department of the Affiliated Hospital. MATERIALS: The experiment was completed in the Imunnohistochemical Laboratory of Basic Medical Institute in Chengde Medical College from February to December in 2004. A total of 30 healthy male Wistar rats were selected, and at random classified as groups of radix astragali pre-treated (radix astragali), ischemic reperfusion and psuedo-operated (control), 10 rats for each group. METHODS: Radix astragali injection was given peritonealy for rats in radix astragali pre-treated group before operation, and the equivalent normal saline was given for those in ischemic reperfusion and psuedo-operated groups. One week later, the model of ischemic reperfusion was set up. After operation the myocardia in marginal zone of ischemic reperfusion were sampled, and the myocardia of the corresponding zone were taken for control group. The method of terminal (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) was used for assay of myocardial apoptosis rate, and the ABC immunohistochemical method was used for assay of myocardial bcl-2 (inhibiting apoptosis gene) and bax (promoting apoptosis gene). MAIN OUTCOME MEASURES: Apoptosis rates, and expression of bcl-2 and bax genes of myocardia RESULTS: ① Apoptosis rate of myocardial cells: The rate in radix astragali group was decreased compared with that in ischemic reperfusion group[ (14.06 ±9.97) %, (19.34±12.30) %, t = 1.863, P < 0.05].② Expression of bcl-2: There was no significant difference between radix astragali and ischemic reperfusion groups[(9.14±4.46) %, (8.99±4.54) %, P < 0.05].③ Expression of bax: The expression in radix astragali group was decreased compared with that in ischemic reperfusion group [(12.65±7.23)%, (18.12±7.92) %, t = 2.096, P < 0.05] CONCLUSION: Pre-treatment with radix astragali can down-regulate the expression of promoting apoptosis gene so as to reduce the rate of myocardial cell apoptosis, hence it can protect the myocardial cells in ischemic reperfusion.
出处 《中国临床康复》 CSCD 北大核心 2005年第23期226-228,共3页 Chinese Journal of Clinical Rehabilitation
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  • 1梁英杰,凌启波.一种快速高敏感的免疫组织化学染色法—LSAB法[J].中华病理学杂志,1993,22(6):369-369. 被引量:71
  • 2汪德清,沈文梅,田亚平,孙仲怡,丛建波,吴可.黄芪有效成分对氧自由基清除作用的ESR研究[J].生物化学与生物物理进展,1996,23(3):260-262. 被引量:126
  • 3Murry CE,Jennings RB,Reimer KA,Precanditioning with ischemia:a delay of lethal cell injury in ischemic myocardium.Circulation 1986;74:1124
  • 4Tomai F,Danesi A.Ghini AS,Crea F,Perino M.Gaspardone A,et al.Effects of KATP channel blockade by glibenclamide on the warm-up phenomenon.Eur Heart J 1999,20(3):196-202.
  • 5Yao Z,Gross GJ.A comparison of adenosine induced cardioprotec tion and ischemic preconditioning in dogn:efficacy,time course and role of K+ATP channela.Circulation 1994;89(3):1229-36.
  • 6Marber MSLatchman DS,Walker JM,Cardiac stress protein elevation 24 hours after brief ischemia or heat-stress is associated with rasistance to myocardial infarction,Circulation 1993;88:1264.
  • 7chults JEJ,Yao Z,Cavera I,et al.Glibenclamide-induced blocicade of iachemic preconditioming is time dependent in intac rat hesrt.Am J physiol 1997;272:H2 607-15.
  • 8Yong ZQ,Nelson L.Induction of 72-kDa heat ahock protein dose not produce second window of ischemic preconditioning in rat heart Am J Physiol Heart Circ Physiol 1999;276(1):224-34.
  • 9Strasser R.Vogt A,Schaper W Myocardial protection by preconditioning.Experimental and clinical significance.Z Kardiol 1996;85(2):79-89.
  • 10Kajstura J,Lab Invest,1996年,74卷,1期,86页

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