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一种内源性的阿德里诺梅杜林可以对抗心血管损伤
Tatsuo Shimosawa1, Yugo Shibagaki, Kotaro Ishibashi
1Department of Nephrology and Endocrinology, Faculty of Medicine, the University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Circulation
|January 5, 2002
概括
内源性腺素 (AM) 通过抑制氧化应激来保护心血管损伤. 使用AM(+/-) 小鼠的研究显示,在接受血管素II和高盐饮食治疗时,心血管损伤和氧化应激标志物增加.
科学领域:
- 心血管科学 心血管科学
- 内分泌学 在内分泌学.
- 分子生物学分子生物学
背景情况:
- 阿德里诺美杜林 (AM) 是一种具有血管扩张和器官保护性能的类激素.
- 亲上腺素N终端20 (PAMP) 与AM联合生产.
- 在体内AM和PAMP的个体生理作用仍然不清楚.
研究的目的:
- 在体内研究内源性上腺素 (AM) 的器官保护作用.
- 阐明AM在血管损伤中由血管素II (Ang II) 和高盐饮食引起的作用.
主要方法:
- 使用了具有中断AM表达 (AM(+/-) 的淘汰赛小鼠.
- 在12天的高盐饮食中服用血管素II (Ang II).
- 评估了心血管变化,氧化应激标志物 (8-基氧氨酸,异素) 和反应性氧物种 (ROS) 的产生.
主要成果:
- 在Ang II/盐治疗后,AM鼠表现出明显的周血管纤维化和冠状动脉内密性增生.
- 抗氧化性压力 (AM) 的小鼠表现出氧化应激标志物的尿排泄增加.
- 在接受AM(+/-) 治疗的小鼠心脏中观察到ROS生成和NAD(P) H氧化酶子单元 (p67phox,gp91phox) 的增加.
结论:
- 内源性AM在预防心血管损伤方面起着保护作用.
- 抗氧化剂的保护机制可能涉及抑制氧化应激的产生.
- 过度产生氧化应激会导致由Ang II/盐负载引起的心血管变化.
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