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慢性心房纤颤犬心房组织中髓过氧物酶的变化 被引量:1

Changes of myeloperoxidase in atrial tissues of dogs with chronic atrial fibrillation
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摘要 目的探讨慢性心房纤颤(房颤)犬心房组织中髓过氧物酶(MPO)的变化及其意义。方法健康杂种犬20条,随机分为房颤组(n=10)和对照组(n=10)。房颤组使用永久起搏器起搏24周,制备房颤犬模型;对照组不置入起搏器。取心房组织标本,分别采用ELISA法、同位素稀释气相色谱质谱法、Masson染色、明胶酶谱法测定MPO含量、3-氯酪氨酸含量、胶原容积分数(CVF)、基质金属蛋白酶-2和9(MMP-2、MMP-9)活性。结果房颤组心房肌组织MPO含量、3-氯酪氨酸含量、CVF、MMP-2和MMP-9活性较对照组显著升高(P<0.05)。MPO含量与CVF显著正相关(P<0.05)。结论 MPO可能是慢性房颤发生和维持的重要介质。 Objective To investigate the changes and significance of myeloperoxidase (MPO) in atrial tissues of dogs with chronic atrial fibrillation. Methods Twenty mongrel dogs were randomly divided into atrial fibr/llation group (n = 10) and control group (n = 10). The High frequency pacing was performed in atrial fibrillation group with permanent pacemaker, but not in the control group. Twenty-four weeks after pacing, atrial tissue was taken. The contents of MPO content and 3-chlorotyrosine were measured by ELISA and stable isotope dilution liquid chromatography with on-line tandem mass spectrometry, respectively. The collagen volume fraction(CVF) and activities of matrix metalloproteinase-2 and 9 ( MMP2, MMP-9) were deter- mined by Masson staining and gelatin zymography, respectively. Results The levels of MPO, 3-chlorotyrosine, CVF and activities of MMP-2 and MMP-9 were significantly higher in atrial fi- brillation group than those in control group (P 〈 0.05 ). The MPO content was significantly cor- related with CVF (P 〈 0.05 ). Conclusion MPO is possibly one of important mediators mech- anistically involved in the initiation and perpetuation of chronic atrial fibrillation.
出处 《哈尔滨医科大学学报》 CAS 北大核心 2013年第1期49-51,55,共4页 Journal of Harbin Medical University
基金 黑龙江省卫生厅科研项目(2007-432)
关键词 心房纤颤 髓过氧物酶 atrial fibrillation canine myeloperoxidase
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  • 1Bontempo LJ, Goralnick E. Atrial fibrillation [ J ]. Emerg Med Clin North Am, 2011,29(4) :747-758.
  • 2Rudolph V, Andri6 RP, Rudolph TK, et al. Myeloperoxidase acts as a pmfibrotic mediator of atrial fibrillation[ J]. Nat Med, 2010, 16(4) :470-474.
  • 3Hazen SL, Crowley JR, Mueller DM, et al. Mass spectrometric quantification of 3-chlorotyrosine in human tissues with attomole sensitivity: a sensitive and specific marker for myeloperoxidase- catalyzed chlorination at sites of inflammation[ J]. Free Radic Biol Med, 1997,23(6) :909-916.
  • 4Loria V, Dato I, Graziani F, et al. Myeloperoxidase: a new bio-marker of inflammation in ischemic heart disease and acute coro- nary syndromes[ J]. Mediators Inflamm, 2008,2008:135625.
  • 5Yamashita T, Sekiguehi A, Iwasaki YK, et al. Recruitment of im- mune cells across atrial endoeardium in human atrial fibrillation [J]. Circ J, 2010,74(2) :262-270.
  • 6Mohammed KS, Kowey PR, Museo S. Adjuvant therapy for atrial fibrillation[ J]. Future Cardiol, 2010,6( 1 ) :67-81.
  • 7Tan AY, Zimetbaum P. Atrial fibrillation and atrial fibrosis[J]. J Cardiovasc Pharmaeol, 2011,57 (6) :625-629.
  • 8Polyakova V, Miyagawa S, Szalay Z, et al. Atrial extracellular matrix remodelling in patients with atrial fibrillation [ J ]. J Cell Mol Med, 2008,12( 1 ) : 189-208.
  • 9Wang Y, Rosen H, Madtes DK, et al. Myeloperoxidase inacti- vates TIMP-1 by oxidizing its N-terminal eystelne residue: an oxi- dative mechanism for regulating proteolysis during inflammation [ J]. J Biol Chem, 2007,282(44) :31826-31834.

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