阿迪波涅丁通过内皮氧化合成酶依赖的机制预防大脑缺血损伤
Masaki Nishimura1, Yasuhiro Izumiya, Akiko Higuchi
1Stroke and Neurovascular Regulation Laboratory, Boston University School of Medicine, Boston, MA, USA.
Circulation
|December 26, 2007
概括
在小鼠中,阿迪波涅丁缺乏会在中风后恶化脑损伤. 补充阿迪波内克丁可以通过增强氧化的产生来减少中风损伤,这表明它可以.
科学领域:
- 心血管研究研究心血管研究
- 神经科学是一个神经科学.
- 内分泌学 在内分泌学.
背景情况:
- 脂肪衍生的蛋白质阿迪波涅丁对心血管健康有好处.
- 低水平的阿迪波涅克丁与较高的死率相关联 缺血性中风后.
- 阿迪波涅丁在缺血性中风中的直接作用尚不清楚.
研究的目的:
- 调查阿迪波涅克丁在急性脑损伤中的因果作用.
- 为了确定阿迪波内克对缺血性中风的影响背后的机制.
主要方法:
- 中脑动脉阻塞 (MCAO) 在缺乏脂肪素 (APN-KO) 和野生型 (WT) 的小鼠中.
- 对脑梗塞和神经系统缺陷的评估.
- 通过腺病毒介导的阿迪波内克丁补充剂.
- 激光斑点流量测量用于大脑血流.
- 免疫组织化学和西式涂抹用于蛋白质分析.
主要成果:
- 与WT小鼠相比,APN-KO小鼠表现出更大的心脏病发作和更严重的神经缺陷.
- 在APN-KO和WT小鼠中,阿迪波涅丁补充剂减少了心脏病发作的大小.
- APN-KO小鼠的脑血流和氧化 (NO) 生产减少了.
- 通过内皮氧化合成酶 (eNOS),阿迪波内克丁的使用增加了NO的产生.
结论:
- 亚迪波内克可以提供对缺血性中风的脑部保护.
- 这种保护作用是由内皮氧化合成酶 (eNOS) 途径介导的.
- 阿迪波内克丁是预防缺血性中风的潜在治疗标.
相关概念视频
Nitric Oxide Signaling Pathway
Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
Ischemic Stroke ll: Pathophysiology
An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
Adrenergic Agonists: Indirect-Acting Agents
Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...

