Related Experiment Video
Updated: Mar 25, 2026
Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
Astragaloside IV improves the isoproterenol-induced vascular dysfunction via attenuating eNOS uncoupling-mediated
Chonghua Xu1, Futian Tang1, Meili Lu1
1Key Laboratory of Cardiovascular and Cerebrovascular Drug Research of Liaoning Province, Liaoning Medical College, Jinzhou 121001, China.
Insights
Astragaloside IV (AsIV) protects against isoproterenol-induced vascular dysfunction by reducing oxidative stress and inflammation. This study shows AsIV improves endothelial function and reduces cardiac hypertrophy markers in rats.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Biochemistry
Background:
- Endothelial dysfunction, driven by oxidative stress and inflammation, contributes to vascular damage in cardiac hypertrophy.
- Previous research indicated Astragaloside IV (AsIV) protects against isoproterenol-induced cardiac hypertrophy in rats.
- The effects of AsIV on aortic function in this model were previously unknown.
Purpose of the Study:
- To investigate the protective effects of Astragaloside IV (AsIV) on isoproterenol-induced vascular dysfunction in Sprague-Dawley rats.
Main Methods:
- Rats were treated with isoproterenol (Iso) alone or in combination with AsIV.
- Vascular responses, oxidative stress markers, nitric oxide (NO) production, and inflammatory pathways were assessed.
Main Results:
- AsIV reduced heart and left ventricular weight/body weight ratios.
- AsIV ameliorated vasoconstriction, suppressed superoxide anion generation, increased endothelial nitric oxide synthase (eNOS) dimer/monomer ratio and tetrahydrobiopterin (BH4) content, and enhanced NO production.
- AsIV reduced peroxynitrite, decreased NF-κB p65 nuclear translocation, increased IκB-α expression, and down-regulated IL-1β, IL-6, and TNF-α mRNA levels.
Conclusions:
- AsIV demonstrates protective effects against isoproterenol-induced vascular dysfunction.
- These benefits are likely mediated by the attenuation of eNOS uncoupling-related oxidative stress.
- Inhibition of reactive oxygen species (ROS)-NF-κB signaling pathways contributes to AsIV's protective mechanism.
Objective:
Oxidative stress and inflammation are regarded as two important triggers of endothelial dysfunction and play pivotal role in progression of vascular damage associated with cardiac hypertrophy. Our previous studies demonstrated that astragaloside IV (AsIV) could protect against cardiac hypertrophy in rats induced by isoproterenol (Iso), but its effects on the aorta are not known. In present study, we aimed to assess the effects of AsIV on Isoinduced vascular dysfunction.
Methods:
Sprague-Dawley (SD) rats were treated with Iso (10mg/kg/d) alone or in combination with AsIV (50mg/kg/d).
Results:
Compared with Isotreated alone, AsIV significantly reduced the ratios of heart weight/body weight and left ventricular weight/body weight. AsIV ameliorated the increased vasoconstriction response to phenylephrine induced by Iso and suppressed superoxide anion generation in rat aorta, increased endothelial nitric oxide synthase (eNOS) dimer/monomer ratio and its critical cofactor tetrahydrobiopterin (BH4) content in aorta as well as the NO production in the serum, reduced the plasmatic peroxynitrite (ONOO-). Moreover, in contrast with Isotreatment alone, AsIV decreased the ratio of nuclear-to-cytosolic protein expression of the NF-κB p65 subunit while enhanced its inhibited protein expression of IκB-α, down-regulated mRNA expression of IL-1β, IL-6 and TNF-α of the aorta.
Conclusions:
The present study suggested that AsIV protects against Isoinduced vascular dysfunction probably via attenuating eNOS uncoupling-mediated oxidative stress and inhibiting ROS-NF-κB pathways.
Related Concept Videos
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
01:26Adrenergic Receptors: β Subtype
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors...
01:31Adrenergic Antagonists: ɑ and β-Receptor Blockers
01:26Heart Failure Drugs: Inotropic Agents
01:23Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
01:30Heart Failure V: Medical Management