过氧化促进与衰老相关的血小板过活化和血栓形成
Sanjana Dayal1, Katina M Wilson, David G Motto
1Department of Internal Medicine, University of Iowa Carver College of Medicine, 200 Hawkins Dr, 3160 ML, Iowa City, IA 52242, USA. sanjana-dayal@uiowa.edu.
Circulation
|February 22, 2013
概括
由于氧化应激,衰老会增加血栓事件. 过度表达谷氨过氧化酶-1 (Gpx1) 通过降低血小板过活和过氧化水平,保护老年小鼠免受血栓形成.
科学领域:
- 老年学是一门学科.
- 心血管生物学 心血管生物学
- 氧化压力研究研究 氧化压力研究
背景情况:
- 血栓事件在老年人群中更常见,但潜在的机制仍然不清楚.
- 氧化应激与与年龄有关的血栓形成风险有关.
- 这项研究调查了抗氧化酶的过度表达是否能防止与年龄相关的血栓形成.
研究的目的:
- 为了测试老年小鼠过度表达谷氨过氧化酶-1 (Gpx1) 的假设,它们被保护免受实验性血栓形成.
- 阐明氧化应激,特别是过氧化在与年龄有关的血栓发作易感性中的作用.
主要方法:
- 阴道动脉的光化学损伤和下静脉结被用来诱导老年和年轻野生型小鼠的血栓形成.
- 过度表达Gpx1 (Gpx1 Tg) 的转基因小鼠与野生型小鼠进行了对血栓敏感性的比较.
- 在老年小鼠中评估了血小板激活标记 (过氧化,纤维素因子结合,αIIbβ3激活) 和NADPH氧化酶活性.
主要成果:
- 与年轻小鼠相比,年龄较大的野生类型小鼠对动脉封闭的时间显著缩短,对静脉血栓形成的易感性增加.
- Gpx1 Tg小鼠没有表现出缩短的闭塞时间或随着年龄的增长而增加静脉血栓形成的易感性.
- 野生型老年小鼠表现出年龄相关的血小板过活化,由过氧化的增加证明,这在Gpx1 Tg小鼠和抗氧化剂中被阻止.
结论:
- 过氧化是老年小鼠血小板过活性的关键媒介.
- 针对氧化应激路径,例如增加谷氨过氧化酶-1,可以减轻与年龄相关的血栓发作易感性.
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