title: Emodin-mediated protection from acute myocardial infarction via inhibition of inflammation and apoptosis in local ischemic myocardium.
abstract: Acute myocardial infarction (AMI) is associated with inflammation and apoptosis. Emodin plays an anti-inflammatory role in several inflammatory diseases. Recent studies have demonstrated that emodin protects against myocardial ischemia/reperfusion injury. However, its mechanism underlying its effects remains unknown. In a murine model of AMI, based on ligation of the left coronary artery, administration of emodin reduced myocardial infarct size (MIS) in a dose-dependent manner. Emodin significantly suppressed TNF-alpha expression and NF-kappaB activation in the local myocardial infarction area. Treatment with emodin inhibited myocardial cell apoptosis by inhibiting caspase-3 activation. Therefore, these studies demonstrate that emodin protects against myocardial cell injury via suppression of local inflammation and apoptosis.
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei, PR China.
authors.forename: Yanxia
authors.initials: Y
authors.lastname: Wu
authors.forename: Xin
authors.initials: X
authors.lastname: Tu
authors.forename: Guosheng
authors.initials: G
authors.lastname: Lin
authors.forename: Hao
authors.initials: H
authors.lastname: Xia
authors.forename: Hao
authors.initials: H
authors.lastname: Huang
authors.forename: Jing
authors.initials: J
authors.lastname: Wan
authors.forename: Zhide
authors.initials: Z
authors.lastname: Cheng
authors.forename: Mengyuan
authors.initials: M
authors.lastname: Liu
authors.forename: Gao
authors.initials: G
authors.lastname: Chen
authors.forename: Haimou
authors.initials: H
authors.lastname: Zhang
authors.forename: Jinrong
authors.initials: J
authors.lastname: Fu
authors.forename: Qian
authors.initials: Q
authors.lastname: Liu
authors.forename: Dong-Xu
authors.initials: DX
authors.lastname: Liu
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology* / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects*; D015153:Blotting, Western; D004195:Disease Models, Animal; D024202:Electrophoretic Mobility Shift Assay; D004642:Emodin / Q000494:pharmacology* / Q000627:therapeutic use; D004797:Enzyme-Linked Immunosorbent Assay; D005434:Flow Cytometry; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009203:Myocardial Infarction / Q000276:immunology / Q000473:pathology / Q000517:prevention & control; D009206:Myocardium / Q000201:enzymology / Q000276:immunology / Q000473:pathology; D016328:NF-kappa B / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000276:immunology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D009195:Peroxidase; D004642:Emodin