Astragaloside IV improves the isoproterenol-induced vascular dysfunction via attenuating eNOS uncoupling-mediated oxidative stress and inhibiting ROS-NF-κB pathways

摘要: Abstract Objective Oxidative stress and inflammation are regarded as two important triggers of endothelial dysfunction play pivotal role in progression vascular damage associated with cardiac hypertrophy. Our previous studies demonstrated that astragaloside IV (AsIV) could protect against hypertrophy rats induced by isoproterenol (Iso), but its effects on the aorta not known. In present study, we aimed to assess AsIV Isoinduced dysfunction. Methods Sprague-Dawley (SD) were treated Iso (10 mg/kg/d) alone or combination (50 mg/kg/d). Results Compared Isotreated alone, significantly reduced ratios heart weight/body weight left ventricular weight. ameliorated increased vasoconstriction response phenylephrine suppressed superoxide anion generation rat aorta, nitric oxide synthase (eNOS) dimer/monomer ratio critical cofactor tetrahydrobiopterin (BH 4 ) content well NO production serum, plasmatic peroxynitrite (ONOO–). Moreover, contrast Isotreatment decreased nuclear-to-cytosolic protein expression NF-κB p65 subunit while enhanced inhibited IκB-α, down-regulated mRNA IL-1β, IL-6 TNF-α aorta. Conclusions The study suggested protects probably via attenuating eNOS uncoupling-mediated oxidative inhibiting ROS-NF-κB pathways.