相关实验视频
Updated: Jul 11, 2026

07:46
Assessing Endothelial Vasodilator Function with the Endo-PAT 2000
Published on: October 15, 2010
在动脉样硬化患者中,循环氧基因酶-1和-2依赖的前环素形成
1Department of Clinical Pharmacology and Surgery, Royal College of Surgeons in Ireland, St Stephens Green, Dublin, Ireland.
Circulation
|August 23, 2000
概括
循环氧化酶-2 (COX-2) 和COX-1有助于增加动脉样硬化中的前环素 (PGI) 含量. 血素A(2) (TXA(2)) 主要由COX-1产生,尼梅苏利德减少PGI(2) 但不是TXA(2).
科学领域:
- 心血管研究研究心血管研究
- 药理学 药理学是指药理学的学科.
- 生物化学 生物化学
背景情况:
- 动脉样硬化与前列腺素 (PGI) 的增加有关,血栓素A (TXA) 和异质素.
- 循环氧化酶-1 (COX-1) 和循环氧化酶-2 (COX-2) 在动脉样硬化中产生这些eicosanoids的特定作用尚未完全阐明.
研究的目的:
- 调查COX-1和COX-2对动脉样硬化患者中PGI(2),TXA(2) 和异质的生产的相对贡献.
- 评估COX抑制对该患者群中的eicosanoid水平的影响.
主要方法:
- 在动脉样硬化组织中使用免疫组织化学分析COX-2mRNA和蛋白质表达.
- 在患有动脉样硬化症的患者中测量TXA的尿中代谢物{2} (11-dehydro-TXB{2}) 和PGI{2} (2,3-dinor-6-keto-PGF{1alpha) 和异素的8-iso-PGF{2alpha).
- 随机试验涉及尼梅苏利德 (一种COX-2抑制剂) 给在接受手术重血管化的患者,有或没有先前的阿司匹林治疗.
主要成果:
- 在动脉样硬化病变中检测到COX-2,局部用于光滑肌细胞和巨细胞,表明其在疾病中的表达.
- 与对照人群相比,动脉样硬化患者的尿液中PGI(2) 和TXA(2) 代谢物水平显著升高.
- 尼梅苏利德治疗显著降低了PGI的代谢物分泌量,降低了46%和手术后的增加,但对TXA的代谢物水平没有显著影响.
- 阿司匹林治疗降低了PGI(2) 和TXA(2) 代谢产物的水平,同时服用尼梅苏利德没有额外的益处.
- 这些干预措施都没有影响尿液中的8-iso-PGF{2α}水平.
结论:
- 无论是COX-1还是COX-2都导致了在动脉样硬化中观察到的高PGI的水平.
- 在动脉样硬化中,TXA(2) 的生成主要由COX-1介导.
- 在动脉样硬化患者中,用尼梅苏利德准COX-2有效降低了PGI(2) 产量,但并没有降低TXA(2) 产量.
相关概念视频
Cofactors and Coenzymes
Enzymes require additional components for proper function. There are two such classes of molecules: cofactors and coenzymes. Cofactors are metallic ions and coenzymes are non-protein organic molecules. Both of these types of helper molecule can be tightly bound to the enzyme or bound only when the substrate binds.
Electron Transport Chain: Complex I and II
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
ROS generation is regulated and maintained at moderate levels necessary...
The Electron Transport Chain
The electron transport chain or oxidative phosphorylation is an exothermic process in which free energy released during electron transfer reactions is coupled to ATP synthesis. This process is a significant source of energy in aerobic cells, and therefore inhibitors of the electron transport chain can be detrimental to the cell's metabolic processes.
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q in...
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q in...
Regulation of Angiogenesis and Blood Supply
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 hydroxylase and factor...
Electron Transport Chain: Complex III and IV
During the electron transport chain, electrons from NADH and FADH2 are first transferred to complexes I and II, respectively. These two complexes then transfer the electrons to ubiquinol, which carries them further to complex III. Complex III passes the electrons across the intermembrane space to Cyt c, which carries them further to complex IV. Complex IV donates electrons to oxygen and reduces it to water. As electrons pass through complexes I, III, and IV, the energy released aids the pumping...
Coronary Artery Disease II: Pathophysiology
Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...

