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阿基纳相互调节氧化合成酶的活性,并有助于老化血管中的内皮功能障碍
Dan E Berkowitz1, Ron White, Dechun Li
1Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Md, USA.
Circulation
|October 1, 2003
概括
老化血管中阿基纳的上调会损害氧化 (NO) 信号传递和内皮功能. 抑制 arginase 恢复 NO 功能,这表明它是与年龄有关的心血管问题的治疗点.
科学领域:
- 心血管生理学心血管生理学
- 生物化学 生化学
- 衰老研究研究 衰老研究
背景情况:
- 异常的L-氨酸和氧化 (NO) 信号与与衰老相关的内皮功能障碍有关.
- 精确的生化机制,特别是阿尔金酶的作用,仍在争论中.
- L-氨酸作为NO合成酶 (NOS) 的前体和氨酶的基质.
研究的目的:
- 通过改变L-氨酸的可用性来研究氨酸酶是否相互调节NOS.
- 为了确定是否在衰老的血管系统中对氨酶进行上调,并有助于降低内皮功能.
主要方法:
- 在大鼠大动脉环中使用了阿基因酶抑制剂,如 (S) -2-甲基) -L-氨酸,HCl (BEC),N-基-nor-L-阿基因 (nor-NOHA) 和二甲基甲 (DFMO).
- 评估了血管扩张,NOS活性和周期性GMP水平.
- 在年轻老老的老鼠血管中测量了阿基因酶活性和表达.
主要成果:
- 在年轻成年大鼠的大动脉环中,阿基纳酶抑制诱导了血管扩张,这种效应取决于完整的内皮和可溶性瓜尼利尔环酶.
- 来自DFMO的血管扩张在老老鼠中明显大于年轻老鼠的甲状腺环.
- 在老血管中,阿基纳酶活性和表达升高,与减少的NOS活性和周期性GMP水平相关. 在老血管中,BEC治疗恢复了依赖L-氨酸的血管松.
结论:
- 氨酸酶活性调节NOS功能,可能通过调节细胞内L-氨酸的可用性.
- 氨酶的上调有助于与衰老相关的内皮功能障碍.
- 阿基纳是一种潜在的治疗点,可以缓解与年龄相关的内皮功能障碍.
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