Related Experiment Video
Updated: Mar 8, 2026
08:21
A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
Published on: October 26, 2020
5.7K
Demethoxycurcumin Preserves Renovascular Function by Downregulating COX-2 Expression in Hypertension
Yingjuan Li1, Danyang Tian2, Chunhua Zhu3
1Department of Geriatrics, Zhongda Hospital, Medical School, Southeast University, 87# Ding Jiaqiao, Nanjing 210009, China.
Oxidative Medicine and Cellular Longevity
|January 21, 2017
Summary
Demethoxycurcumin (DMC), derived from turmeric, improves blood vessel function in hypertension by reducing cyclooxygenase-2 (COX-2) expression. This natural compound offers a potential therapeutic strategy for hypertension-related endothelial dysfunction.
Area of Science:
- Pharmacology
- Cardiovascular Biology
- Natural Products Chemistry
Background:
- Hypertension often leads to endothelial dysfunction, characterized by impaired blood vessel relaxation and increased contraction.
- This dysfunction is frequently linked to elevated cyclooxygenase-2 (COX-2) activity, an enzyme induced by inflammation.
- Demethoxycurcumin (DMC), a curcuminoid from *Curcuma longa*, exhibits anti-inflammatory properties.
Purpose of the Study:
- To investigate the potential of DMC in ameliorating hypertension-induced endothelial dysfunction.
- To determine if DMC modulates cyclooxygenase-2 (COX-2) expression and activity in hypertensive models.
- To assess DMC's effects on vascular tone, nitric oxide (NO) generation, and endothelial nitric oxide synthase (eNOS) phosphorylation.
Main Methods:
- Isometric tension measurements in isolated rat renal arteries (SHR and WKY) and human umbilical vein endothelial cells (HUVECs).
- In vivo and ex vivo administration of DMC and celecoxib (a COX-2 inhibitor).
- Assessment of COX-2 expression, nitric oxide (NO) production, and eNOS phosphorylation (Ser1177) following angiotensin II (Ang II) stimulation.
Main Results:
- DMC treatment restored normal endothelium-dependent relaxations and contractions in hypertensive rat renal arteries.
- DMC normalized elevated COX-2 expression in the renal arteries of spontaneously hypertensive rats (SHR) and hypertensive patients.
- DMC prevented angiotensin II-induced endothelial dysfunction in Wistar-Kyoto rats and normalized NO generation and eNOS phosphorylation in HUVECs.
Conclusions:
- Demethoxycurcumin (DMC) effectively improves endothelial function in hypertension by suppressing COX-2 expression.
- DMC mitigates exaggerated vasoconstriction and restores vasodilation, offering a potential therapeutic avenue.
- The findings highlight DMC's role in managing hypertension-associated vascular complications through COX-2 modulation.
More Related Videos
Related Concept Videos
01:23Antihypertensive Drugs: Vasodilators
2.4K
Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
2.4K
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
1.3K
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
1.3K
01:30Antihypertensive Drugs: Angiotensin II Receptor Blockers
2.9K
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...
2.9K
01:29Hypertension II: Pathophysiology
1.3K
Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
1.3K
01:25Antihypertensive Drugs: Direct Renin Inhibitors
1.7K
The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
1.7K
01:16Antihypertensive Drugs: Action of Diuretics
2.6K
Diuretics are antihypertensive drugs used to treat hypertension resulting from sodium and water retention. Sodium, vital for fluid balance and nerve or muscle function, is regulated by the kidneys through millions of nephrons. Blood enters nephrons via afferent arterioles, which branch into capillaries called glomeruli. These filter blood plasma, allowing water and solutes, like sodium ions, to pass through capillary walls into Bowman's capsule. The filtrate then flows through various...
2.6K