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首乌丹参方预处理对大鼠心肌缺血再灌注损伤PKC与iNOS mRNA表达的影响 被引量:7

Effect of Gold Theragran Salvia Miltiorrhiza Prescription Pretreatment on Expression of Protein Kinase C and iNOS in mRNA Level of Myocardial Ischemia Reperfusion Injury in Rats
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摘要 目的观察首乌丹参方(GTSMP)对大鼠心肌缺血再灌注损伤(I/R)保护作用。方法将实验大鼠分为假手术组、模型组、首乌丹参方高剂量组(9g生药/kg)、首乌丹参方中剂量组(4.5g生药/kg)、首乌丹参方低剂量组(2.25g生药/kg)、阳性对照药复方丹参滴丸组(4.5g生药/kg)、工具对照药消心痛组(1.67mg/kg),共7组。采用结扎大鼠冠状动脉前降支30min/开放120min建立心肌I/R模型。通过RT-PCR分子生物学方法,观察蛋白激酶C(PKC) mRNA和iNOS mRNA的表达情况以及首乌丹参方预处理对其的影响。结果与假手术组相比,模型组和首乌丹参方各组PKC mRNA表达均有所下降;与模型组相比,首乌丹参方中剂量组、复方丹参滴丸组和消心痛组表达上调,均表现出显著性差异,首乌丹参方高剂量组及低剂量组也能促进PKC mRNA的表达,但没有显著性差异;假手术组心肌iNOS mRNA弱表达,模型组呈现高表达,首乌丹参方可下调iNOS mRNA基因表达。结论首乌丹参方预处理可促进I/R的大鼠心肌的PKC表达,下调I/R大鼠心肌iNOS mRNA的表达;其通过激动PKC,使心肌组织iNOS mRNA弱表达,可能是首乌丹参方对缺血再灌注损伤的心肌的保护效应机制之一。 Objective To observe the protective mechanism against experimental myocardial ischemia-reperfusion rats pretreated with Gold Theragran Salvia miltiorrhiza prescription (GTSMP). Methods The rats were divided into seven groups: sham group, model group, GTSMP high-dose group(9g/kg), moderate-dose group(4.5/kg) and low-dose group (2.25/kg), Isorbil (1.67mg/kg) and compound Danshen dripping pill (4.5g/kg) as control groups. The rat model of IR was built by ligating the left anterior descending coronary, artery for 30 minutes followed by 2 hours of reperfusion, to observe the expression mRNA of protein kinase C and iNOS and effect of pretreated with GTSMP to I/R rats by the method of RT-PCR. Results The expression of PKC mRNA of model group and every GTSMP group was down-regulated compared with that of sham operation group. Compared with model group, the expression of PKC mRNA of GTSMP moderate dose treated group, compound Dan-shen dripping pill treated group and Isorbil group was up-regulated significantly. GTSMP high-dose group and GTSMP low-dose group can also promote the expression, but they did not have significant differences. The expression of iNOS mRNA in model group was up-regulated compared with sham group and in every GTSMP group; the expression of iNOS mRNA was down-regulated compared with model group. Conclusion GTSMP pretreatment can up-regulate the expression of protein kinase C-mRNA and down-regulate iNOS mRNA on IR in rats. The possible protective mechanism may up-regulate expressions of the protein kinase C-mRNA and down- regulate the expression of iNOS mRNA.
出处 《上海中医药杂志》 北大核心 2007年第10期75-78,共4页 Shanghai Journal of Traditional Chinese Medicine
基金 天津市科技发展基础研究重点资助项目(033802111) 天津市高等学校科技发展基金资助项目(20030101)
关键词 首乌丹参方 缺血再灌注 蛋白激酶-C 诱生型一氧化氮合酶 Gold theragran salvia miltion'hiza prescription(GTSMP) isehemia reperfusion(I/R), protein kinase C (PKC) iNOS
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参考文献11

  • 1Yao Z,Gross GJ.A comparision of adenosine induced cardioprotection and ischemic preconditioning in dogs:efficacy,time course and role of K+-ATP channels[J].Circulation,1994,89(3):1229-1236.
  • 2Cave AC,Collis CS,Downey JM,et al.Improved functional recovery by ischaemic preconditioning is not mediated by adenosine in the globally ischaemic isolated rat heart[J].Cardiovasc Res,1993,27(4):663-668.
  • 3高秀梅,张伯礼,商洪才,王怡,郭利平,张萌,史红,刘密新.复方丹参对缺血预适应大鼠心肌蛋白激酶C表达的影响[J].中草药,2003,34(10):933-935. 被引量:16
  • 4Nishizuka Y.Protein kinase 5,protein kinase C and lipid sigualing for sustained cellular responses[J].FASEB J,1995,9(5):484-494.
  • 5Hu K,Duan D,Li GR,et al.Protein kinase C activates ATP-sensitive K1 current in human and rabbit ventricu-larmyocytes[J].Circ Res,1996,78(3):492-498.
  • 6Rybin VO,Steinberg SF.Protein kinase C isoform expression and regulation in the developing rat heart[J].Citc Res,1994,74(2):299-309.
  • 7Suzuki H,Wildhirt SM,Dudek RR,et al.Induction of apoptosis in myocardial infarction and its possible relationship to nitric oxide synthase in macrophages[J].Tissue Cell,1996,28(1):89-97.
  • 8Schulz R,Wambolt R.Inhibition of nitric oxide synthesis protects the isolated working rabbit heart from ischemia-repedusion injury[J].Cardiovasc Res,1995,30(3):432-439.
  • 9Brady AJ,Poole-Wilson PA,Harding SE,et al.Nitric oxide production within cardiac myocytos reduces their contractility in endotoxemia[J].Am J Physiol,1992,263(6 Pt 2):H1963-H1966.
  • 10Gardiner SM,Kemp PA,March JE,et al.Cardiac and regional haemedynamics,inducible nitric oxide synthase(NOS)activity,and the effects of NOS inhibitom in conscious,endotoxaemic rats[J].Br J Pharmacol,1995,116(3):2005-2016.

二级参考文献10

  • 1[1]Moncada S,Palmer RM,Higgs EA. Nitric oxide:physiology,pathophysiology,and pharmacology[J]. Pharmacol Rev,1991,43:109-142.
  • 2[2]Ikeda U,Maeda Y,Kawahara Y,et al. Molecular mechanisms and therapeutic strategies related to nitric oxide[J]. FASEB J,1995,9:1319-1330.
  • 3[3]Vallance P,Collier J,Moncada S. Effects of endothelium-derived nitric oxide on peripheral arteriolar tone in man[J]. Lancet,1989,2.
  • 4[4]Brady AJ,Poole-Wilson PA,Harding SE,et al. Nitric oxide production within cardiac myocytes reduces their contractility in endotoxemia[J]. Am J Physiol,1992,263:H1963-H1966.
  • 5[5]Gardiner SM,Kemp PA,March JE,et al. Cardiac and regional haemodynamics,inducible nitric oxide synthase (NOS) activity,and the effects of NOS inhibitors in conscious,endotoxaemic rats[J]. Br J Pharmacol,1995,116:2005-2016.
  • 6[6]Brady AJB,Poole-Wilson PA,Harding SE,et al. Nitric oxide production within cardiac myocytes reduces their contractility in endotoxemia[J]. Am J Physiol,1992,263:H1963-H1966.
  • 7[7]McKenna TM,Li S,Tao S. PKC mediates LPS- and phorbol-induced cardiac cell nitric oxide synthase activity and hypocontractility[J]. Am J Physiol,1995,269:1891-1898.
  • 8[8]Qingping Feng,Xiangru Lu,Douglas L. Jones,et al. Increased inducible nitric oxide synthase expression contributes to myocardial dysfunction and higher mortality after myocardial infarction in mice.
  • 9[9]Hibbs JB Jr,Taintor RR,Vavrin Z,et al. Synthesis of nitric oxide from a terminal guanidino nitrogen atom of L-arginine:a molecular mechanism regulating cellular proliferation that targets intracellular iron. In:Moncada S,Higgs EA,eds. Nitric Oxide From L-Arginine:A Bioregulatory System. Amsterdam,Netherlands:Excerpta Medica.
  • 10Nishizuka Y. Protein kinase 5, protein kinase C and lipid signaling for sustained cellular responses[J]. FASEB J, 1995,9(5):484-494.

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