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抗氧化剂干预减弱了高胆固醇血中心肌新血管化的作用.

Xiang-Yang Zhu1, Martin Rodriguez-Porcel, Michael D Bentley

  • 1Department of Internal Medicine, Division of Hypertension, Mayo Clinic College of Medicine, Rochester, Minn 55905, USA.

Circulation
|March 31, 2004
PubMed
概括

在高胆固醇血症 (HC) 中,慢性抗氧化剂干预使心肌微血管变化正常化,并保持关键生长因子表达. 这项研究强调了抗氧化剂在早期动脉样硬化中对氧化应激的保护作用.

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科学领域:

  • 心血管研究研究心血管研究
  • 氧化压力生物学 氧化压力生物学
  • 动脉样硬化病理生理病理学

背景情况:

  • 高胆固醇血症 (HC) 和动脉样硬化诱导氧化应激,内皮功能障碍和缺血,可能导致心肌新血管化.
  • 增长因子表达,包括缺氧诱导因子 (HIF) -1alpha和血管内皮生长因子 (VEGF),可能会受到这些条件的调节.
  • 这项研究研究了慢性抗氧化剂干预在高胆固醇模型中对这些过程的影响.

研究的目的:

  • 为了测试这种假设,慢性抗氧化剂干预高胆固醇血症减弱心肌新血管化.
  • 为了确定抗氧化剂治疗是否在HC的背景下保留HIF-1alpha和VEGF的表达.
  • 阐明氧化应激在早期动脉动脉生成期间调节心肌微血管结构中的作用.

主要方法:

  • 一项为期12周的研究涉及三组猪:正常饮食,2%的HC饮食和HC与抗氧化剂补充剂 (维生素E和C).
  • 使用3D微型CT扫描分析心肌样本,以评估微血管空间密度和扭曲度.
  • 在心肌组织中量化VEGF mRNA,VEGF和VEGF受体-1蛋白水平,HIF-1alpha,尼甲酸氨酸和超氧化物失调酶 (SOD).

主要成果:

  • 高胆固醇血症显著增加了心下微血管密度和动脉曲,与正常对照相比.
  • 抗氧化剂补充剂在HC动物中使微血管密度和扭曲度正常化.
  • HC诱导了VEGF,HIF-1alpha和尼铁的上调,同时降低了SOD;这些变化被抗氧化剂治疗逆转.

结论:

  • 高胆固醇血症改变心肌微血管结构,与增加的HIF-1alpha和VEGF表达相关.
  • 抗氧化剂的干预有效地减轻了这些微血管变化和HC的生长因子改变.
  • 增加的氧化应激在动脉动脉的早期阶段在调节心肌微血管架构方面发挥着重要作用.