title: Kaempferide-7-O-(4"-O-acetylrhamnosyl)-3-O-rutinoside reduces myocardial infarction size after coronary artery ligation in rats.
abstract: Kaempferide-7-O-(4"-O-acetylrhamnosyl)-3-O-rutinoside (A-F-B) is a novel flavonoid extracted from the leaves of Actinidia kolomikta. We recently reported that A-F-B administration could improve lipid profiles. A-F-B actions are associated with regulating the activities of PAP and HMG-CoA reductase in hepatic tissue. This study evaluated the effects of A-F-B on acute myocardial infarction (AMI) in rats. An AMI model was established by ligating the left anterior descending coronary artery. The myocardial infarct size (MIS), creatine kinase (CK-MB) activity, troponin T level, endothelial nitric oxide synthase (eNOS) activity, superoxide dismutase (SOD) activity, catalase activity, malondialdehyde (MDA) content, nitric oxide (NO) content were measured. The results showed that the groups treated with A-F-B showed a dose-dependent reduction in MIS. A-F-B markedly inhibited the elevation of the activity of CK-MB, troponin T level, and the content of MDA induced by AMI. A-F-B also showed a capacity to increase the activities of SOD, catalase, and eNOS. The NO content in A-F-B-treated groups also augmented. The findings suggest that A-F-B exerted cardioprotective effects against acute myocardial ischemic injury by regulating antioxidative enzymes activity and endothelial nitric oxide synthase activity.
authors.affiliation: The First Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
authors.forename: Gaowa
authors.initials: G
authors.lastname: Eerduna
authors.forename: Dongsheng
authors.initials: D
authors.lastname: Wei
authors.forename: Xiaofeng
authors.initials: X
authors.lastname: Yu
authors.forename: Shaochun
authors.initials: S
authors.lastname: Qu
authors.forename: Dayuan
authors.initials: D
authors.lastname: Sui
mesh_terms: D000208:Acute Disease; D000818:Animals; D002316:Cardiotonic Agents; D002374:Catalase / Q000378:metabolism; D003331:Coronary Vessels / Q000473:pathology*; D003402:Creatine Kinase / Q000378:metabolism; D006027:Glycosides / Q000494:pharmacology*; D007202:Indicators and Reagents; D044949:Kaempferols / Q000494:pharmacology*; D008026:Ligation; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000473:pathology*; D017202:Myocardial Ischemia / Q000188:drug therapy / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D009569:Nitric Oxide / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D013482:Superoxide Dismutase / Q000378:metabolism; D020107:Troponin T / Q000097:blood
chemical_list: D002316:Cardiotonic Agents; D006027:Glycosides; D007202:Indicators and Reagents; D044949:Kaempferols; D020107:Troponin T; C571783:kaempferide-7-O-(4''-O-acetylrhamnosyl)-3-O-rutinoside; D009569:Nitric Oxide; D008315:Malondialdehyde; D002374:Catalase; D052250:Nitric Oxide Synthase Type III; D013482:Superoxide Dismutase; D003402:Creatine Kinase