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骨髓氧化酶产生的氧化剂调节左心室重塑,但不能调节心肌梗塞后的心脏病发作的大小
Nikolay Vasilyev1, Timothy Williams, Marie-Luise Brennan
1Department of Cell Biology, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.
Circulation
|November 4, 2005
概括
心脏病发作 (心肌梗塞) 后的炎症会使心脏功能恶化. 骨髓氧化酶 (MPO) 产生的化物,而不是心脏病发作大小,驱动不良的心脏重塑和左心室功能受损.
科学领域:
- 心血管生物学 心血管生物学
- 炎症研究 炎症研究
- 氧化压力是一种氧化压力.
背景情况:
- 心肌梗塞 (MI) 后的炎症与左心室 (LV) 功能和结果差异有关.
- 炎症影响 LV 功能的确切机制,特别是关于心脏病发作大小和 LV 重塑的具体机制,仍然不清楚.
- 氧化压力可能会产生细胞毒性化物,可能会影响重塑和心脏病发作的大小.
研究的目的:
- 调查骨髓氧化酶 (MPO) 在MI期间产生细胞毒性化物中的作用.
- 确定MPO产生的氧化剂对心脏病发作大小和LV重塑在缺血/再输血MI模型中的功能影响.
主要方法:
- 评估了氨基酸的MPO氧化产物在血管细胞类型中的细胞毒性.
- 利用质谱法在小鼠MI心肌组织中识别MPO产生的化物 (甲,烯).
- 在缺血症/再输液损伤后,对MPO-null和野生型小鼠的LV重塑和功能进行比较.
主要成果:
- 甘氨酸和氨酸的MPO氧化产生了最具有细胞毒性 aldehydes (甲和acrolein).
- 骨髓氧化酶 (MPO) 被证实是MI心肌组织中这些化物的主要酶源.
- 与野生型小鼠相比,MPO-null小鼠显著减少了LV扩张 (35.1%) 和改善了LV功能 (52.2%) ,心脏病发作的大小没有差异.
结论:
- 对心脏病发作大小和LV重塑的炎症影响是不同的.
- 由MPO产生的氧化剂不会显著影响MI后心肌缩.
- 由MPO产生的氧化剂对MI后的LV重塑和功能产生不利影响.
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