title: Apocynin ameliorates pressure overload-induced cardiac remodeling by inhibiting oxidative stress and apoptosis.
abstract: Oxidative stress plays an important role in pressure overload-induced cardiac remodeling. The purpose of this study was to determine whether apocynin, a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, attenuates pressure overload-induced cardiac remodeling in rats. After abdominal aorta constriction, the surviving rats were randomly divided into four groups: sham group, abdominal aorta constriction group, apocynin group, captopril group. Left ventricular pathological changes were studied using Masson's trichrome staining. Metalloproteinase-2 (MMP-2) levels in the left ventricle were analyzed by western blot and gelatin zymography. Oxidative stress and apoptotic index were also examined in cardiomyocytes using dihydroethidium and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), respectively. Our results showed that abdominal aorta constriction significantly caused excess collagen deposition and cardiac insult. Treatment with apocynin significantly inhibited deposition of collagen and reduced the level of MMP-2. Furthermore, apocynin also decreased the NADPH oxidase activity, reactive oxygen species production and cardiomyocyte apoptotic index. Interestingly, apocynin only inhibited NADPH oxidase activity without affecting its expression or the level of angiotensin II in the left ventricle. In conclusion, apocynin reduced collagen deposition, oxidative stress, and inhibited apoptosis, ultimately ameliorating cardiac remodeling by mechanisms that are independent of the renin-angiotensin system.
authors: Department of Physiology and Pathophysiology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi Province, China, Department of Pharmacology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi Province, China, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi Province, China. lichunfang626@126.com.
authors: J-J
authors: JJ
authors: Liu
authors: Y
authors: Y
authors: Lu
authors: N-N
authors: NN
authors: Ping
authors: X
authors: X
authors: Li
authors: Y-X
authors: YX
authors: Lin
authors: C-F
authors: CF
authors: Li
mesh_terms: D000098:Acetophenones / Q000494:pharmacology*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000037:antagonists & inhibitors / Q000378:metabolism; D020257:Ventricular Remodeling / Q000187:drug effects* / Q000502:physiology
chemical_list: D000098:Acetophenones; D000975:Antioxidants; D017382:Reactive Oxygen Species; C056165:acetovanillone