相关实验视频
Updated: Jul 6, 2025
07:42
Nerve-sparing Mid-urethral Obstruction NeMO in Female Small Rodents
Published on: April 25, 2017
9.6K
由于长期的膀出口阻塞引起的膀不活性的 ангиопоэтин表达减少
Jae Heon Kim1, Hee Jo Yang2, Hong Jun Lee3
1Department of Urology, Soonchunhyang University Seoul Hospital, Soonchunhyang University School of Medicine, Seoul, Korea.
International neurourology journal
|January 3, 2024
概括
慢性膀输出阻塞 (BOO) 在老鼠导致血管蛋白的表达减少,可能导致膀缺血和纤维化. 这项研究提供了对低活性膀疾病过程的见解.
科学领域:
- 泌尿器科 泌尿器科 泌尿器科 泌尿器科
- 血管生物学 血管生物学
- 分子生物学分子生物学
背景情况:
- 膀缺血可能发生在慢性膀输出阻塞 (BOO) 期间新血管化无法满足氧气需求时.
- 膀功能低下是由于BOO导致膀功能受损的潜在后果.
研究的目的:
- 为了研究由慢性BOO引起的膀功能低下的老鼠模型中的血管新生生长因子表达的改变.
- 探索BOO,缺氧和血管生成因子变化的关系.
主要方法:
- 20只雌性Sprague-Dawley大鼠被分为对照组,假手术组和BOO组 (随访1周和8周).
- 膀功能通过囊泡测量进行评估;组织分析包括血管生成相关生长因子的实时PCR和低氧信号通路阵列.
主要成果:
- 8周的BOO导致膀功能异常 (缩短交收缩间隔,降低排泄压力,增加余尿) 和高的缺氧诱导因子-1α.
- 血管内皮生长因子 (VEGF) 和VEGF受体mRNA水平与对照水平相比,但血管新生素/结合受体mRNA最初增加,然后减少.
- 对·威勒布兰德因子的阳性染色减少表明BOO大鼠的血管数量减少,同时出现缺氧信号通路的改变.
结论:
- 在大鼠的手术BOO诱导了低活性膀与降低的血管蛋白表达.
- 这种降低的血管蛋白可能会导致BOO中观察到的内脏缺血和纤维化.
- 这些发现提高了对BOO病理生理学的理解,并可能指导手术干预的时间.
相关概念视频
01:24Regulation of Angiogenesis and Blood Supply
2.6K
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.6K
01:30Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
645
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...
645
01:10Mechanism of Angiogenesis
5.5K
Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
5.5K
01:30Antihypertensive Drugs: Angiotensin II Receptor Blockers
735
In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
735