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Renal Corpuscle
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在阿波利波蛋白E-null小鼠中,血管激素II类型2受体的删除导致过度动脉样硬化
Masaru Iwai1, Rui Chen, Zhen Li
1Division of Medical Biochemistry and Cardiovascular Biology, Department of Molecular and Cellular Biology, Ehime University School of Medicine, Shitsukawa, Tohon, Ehime 791-0295, Japan.
Circulation
|September 8, 2005
概括
ангиотензин II 2 型受体刺激通过抑制氧化应激来减少动脉样硬化. 这表明瓦尔萨尔坦.
科学领域:
- 心血管研究研究心血管研究
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 动脉样硬化包括氧化应激.
- 血管激素II型2 (AT2) 受体在动脉样硬化中的作用尚不清楚.
- 使用AT2受体/脂蛋白E (ApoE) 双击 (DKO) 鼠标来研究这一作用.
研究的目的:
- 探索AT2受体在动脉样硬化中的作用.
- 研究AT2受体对动脉样硬化的氧化应激的影响.
- 了解AT2受体介导作用的机制.
主要方法:
- 在使用高胆固醇饮食的ApoE-knockout (KO) 和AT2/ApoE-DKO小鼠中诱导了动脉样硬化.
- 测量了氧化应激标志物 (超氧化物产生,NADPH氧化酶活性,p47phox表达).
- 在体内和体外检查了Angiotensin II型1 (AT1) 受体阻塞剂 (瓦尔萨坦) 和AT2受体阻塞剂 (PD123319) 的作用.
主要成果:
- 与ApoE-KO小鼠相比,AT2/ApoE-DKO小鼠显示出夸张的动脉样硬化病变和增加的氧化应激.
- 瓦尔萨坦抑制了病变形成和氧化应激,但这些效应在AT2/ApoE-DKO小鼠中较弱.
- 在培养细胞中,Ang II诱导的NADPH氧化酶活性被瓦尔萨坦抑制,但被PD123319增强,表明AT2受体介导的抗氧化作用.
结论:
- 刺激AT2受体可以通过抑制氧化应激来减轻动脉样硬化.
- 瓦尔沙坦的抗动脉样硬化作用可能涉及未结合的Ang II的AT2受体刺激.
- 向AT2受体可能是动脉样硬化治疗的治疗策略.
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