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脓毒症大鼠心肌细胞凋亡和p53蛋白表达相关性的研究

Correlation between the Expression of the p53 Protein and Myocardial Apoptosis in Septic Rats
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摘要 目的研究脓毒症大鼠心肌细胞凋亡的变化及其与p53蛋白表达的关系。方法以盲肠结扎穿刺法复制脓毒症大鼠模型,以电镜和凋亡原位末端标记法(TUNEL法)检测其心肌细胞凋亡变化,用免疫组化方法检测p53蛋白的表达。结果一定时间内脓毒症大鼠心肌细胞凋亡率均明显高于正常对照组和假手术对照组(P均<0.05),p53蛋白表达阳性数均较正常对照或假手术组明显升高(P均<0.05),其变化与TUNEL法检测凋亡的结果一致(P<0.05)。结论细胞凋亡可能是脓毒症时心肌损害的机制之一,其调控基因p53的改变或许可以作为脓毒症病情改变的标志,可利用它对脓毒症进行干预,以改善脓毒症的预后。 Objective To study the correlation between myocardial apoptosis and the expression of the p53 protein in septic rats. Method The sepsis model was constructed by cecal ligation and puncture. The myocardial apoptosis was detected by electron microscopy and TdT-mediated dUTP Nick End Labeling (TUNEL). The p53 protein was detected by immunohistochemistry method. SPSS 10.0 statistical software was used to analyzed the data. Result Within certain period, the myocardial apoptosis rates and expression of p53 protein in septic rats were higher than that in normal and sham-operated control group (P〈0.05). The trend was parallel with the change of the results of TUNEL. Conclusion Myocardial apoptosis may contribute to the myocardial injury in sepsis. The p53 level may be able to indicate myocardial injury. The p53 gene may be used as a target for treating and prognosis of sepsis.
出处 《热带医学杂志》 CAS 2007年第6期572-574,579,共4页 Journal of Tropical Medicine
基金 广东省科技计划项目(No.2004B30601002) 广州市科委重点课题基金(No.2001-Z-130-02)
关键词 脓毒症 细胞凋亡 心肌损害 P53 sepsis cell apoptosis myocardial injury p53
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参考文献11

  • 1KUMAR A,HAERY C,PARRILLO JE.Myocardial dysfunction in septic shock[J].Crit Care Clin,2000,16:251-287.
  • 2马中富,乐胜,梁艳冰,詹红,唐皓,荆小莉.p38丝裂原活化蛋白激酶抑制剂对脓毒症大鼠多器官损伤的保护作用研究[J].中国危重病急救医学,2005,17(4):211-213. 被引量:18
  • 3GIROIR BP,STROMBERG D.Myocardial depression versus myocardial destruction:Integrating the muhiple mechanisms of myocardial dysfunction during sepsis[J].Crit Care Med,2000,28(8):3111-3112.
  • 4LANCEL S,PETILLOT P,FAVORY R,et al.Expression of apoptosis regulatory factors during myocardial dysfunction in endotoxemic rats[J].Crit Care Med,2005,33:492-496.
  • 5ZHAO Z,MORRIS CD.Inhibition of myocardial apoptosis reduces infarct size and improves regional contractile dysfunction during reperfusion[J].Cardiovascular Res,2003(59):132-142.
  • 6WATTS JA,KLINE JA.Metabolic dysfunction and depletion of mitochondria in hearts of septic rats[J].Mol and Cell Cardiol,2004,36:141-150.
  • 7HOTCHKISS RS,TINSLEY KW.p53-dependent andindependent pathways of apoptotic cell death in sepsis[J].J Immunol,2000,164:3675-3680.
  • 8MCDONALD TE,GRINMAN MN.Endotoxin infusion in rats induces apoptotic and survival pathways in hearts[J].Am J Physiol Heart Circ Physiol,2000,279:H2053-H2061.
  • 9MITCHELL RA,LIAO H,CHESNEY J.Macrophage migration inhibitory factor(MIF)sustains macrophage prainflammatory function by inhibiting p53:Regulatory Me in the innate immune response[J].PNAS,2002,99:345-350.
  • 10MINNICH DJ,D'AMORE J.Anti-cytokine and antiinflammatory therapies for the treatment of severe sepsis:progress and pitfalls[J].Proc Nutr Soc,2004:63:437-441.

二级参考文献12

  • 1Hale K K,Trollinger D,Rihanek M,et al.Differential expression and activation of p38 mitogen-activated protein kinase alpha,beta,gamma,and beta in inflammatory cell lineages[J].J Immunol 1999,162:4246-4252.
  • 2Symons J A,Young P R,Duff G W.Soluble typeⅡ interleukin-1(IL1) receptor binds and blocks processing of IL-1 beta precursor and loses affinity for IL-1 receptor antagonist[J].Proc Natl Acad Sci USA,1995,92:1714-1718.
  • 3Reinhart K,Wiegand Lohnert C,Grimminger F,et al.Assessment of the safety and efficacy of the monoclonal anti tumor necrosis factor antibody fragment,MAK195F,in patients with sepsis and septic shock:a multicenter,randomized,placebo controlled,dose ranging study[J].Crit Care Med,1996,24:742-773.
  • 4Lee J C,Kassis S,Kumar S,et al.p38 mitogen activated protein kinase inhibitor-mechanisms and therapeutic potentials[J].Pharmacol Ther,1999,82:389-397.
  • 5Obata T,Brown G E,Yaffe M B.MAP kinase pathways activation bu stress:the p38 MAPK pathway[J].Crit Care Med,2000,28:N67-N77.
  • 6Branger J,van den Blink B,Weijer S,et al.Anti-inflammatory effects of a p38 mitogen-activated protein kinase inhibitor during human endotoxemia[J].J Immunol,2002,168:4070-4077.
  • 7Nick J A,Avdi N J,Young S K,et al.An intracellular signaling pathway linhing lipopolysaccaride stimulation to cellular responses of the human neitrophil:thr p38 MAP kinase cascade and its functional significance[J].Chest,1999,116(1Suppl):54S-55S.
  • 8Ono K,Han J.The p38 signal transduction pathway:activation and function[J].Cell Signal,2000,12:1.
  • 9姚咏明,盛志勇.MODS抗炎治疗研究的反思[J].中国危重病急救医学,1999,11(8):456-458. 被引量:74
  • 10梁华平,王正国,朱佩芳.针对SIRS的新型抗炎靶点及抗炎策略研究进展——从炎症介质到核因子-κB[J].中国危重病急救医学,2001,13(11):649-652. 被引量:34

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