title: Protective effects of caffeic acid phenethyl ester on skeletal muscle ischemia-reperfusion injury in rats.
abstract: There is a great evidence that reactive oxygen species (ROS) play an important role in the pathophysiology of ischemia-reperfusion (I/R) injury in skeletal muscle. Caffeic acid phenethyl ester (CAPE) is a component of honeybee propolis. It has antioxidant, anti-inflammatory and free radical scavenger properties. The aim of this study is to determine the protective effects of CAPE against I/R injury in respect of protein oxidation, neutrophil in filtration, and the activities of xanthine oxidase (XO) and adenosine deaminase (AD) on an in vivo model of skeletal muscle I/R injury. Rats were divided into three equal groups each consisting of six rats: Sham operation, I/R, and I/R plus CAPE (I/R+CAPE) groups. CAPE was administered intraperitoneally 60 min before the beginning of the reperfusion. At the end of experimental procedure, blood and gastrocnemius muscle tissues were used for biochemical analyses. Tissue protein carbonyl (PC) levels and the activities of XO, myeloperoxidase (MPO) and AD in I/R group were significantly higher than that of control (p < 0.01, p < 0.05, p < 0.01, p < 0.005, respectively). Administration of CAPE significantly decreased tissue PC levels, MPO and XO activities in skeletal muscle compared to I/R group (p < 0.01, p < 0.05, p < 0.05, respectively). In addition, plasma creatine phosphokinase (CPK), XO and AD activities were decreased in I/R+CAPE group compared to I/R group (p < 0.05, p < 0.05, p < 0.001). The results of this study revealed that free radical attacks may play an important role in the pathogenesis of skeletal muscle I/R injury. Also, the potent free radical scavenger compound, CAPE, may have protective potential in this process. Therefore, it can be speculated that CAPE or other antioxidant agents may be useful in the treatment of I/R injury as well as diffused traumatic injury of skeletal muscle.
authors.affiliation: Departments of Anatomy, Gaziosmanpasa University Faculty of Medicine, Dekanlik Binasi, Tokat, Turkey. mdbirsen@hotmail.com
authors.forename: Birsen
authors.initials: B
authors.lastname: Ozyurt
authors.forename: Mustafa
authors.initials: M
authors.lastname: Iraz
authors.forename: Kenan
authors.initials: K
authors.lastname: Koca
authors.forename: Huseyin
authors.initials: H
authors.lastname: Ozyurt
authors.forename: Semsettin
authors.initials: S
authors.lastname: Sahin
mesh_terms: D000243:Adenosine Deaminase / Q000097:blood; D000818:Animals; D002109:Caffeic Acids / Q000494:pharmacology*; D003402:Creatine Kinase / Q000097:blood; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000473:pathology*; D009195:Peroxidase / Q000378:metabolism; D010626:Phenylethyl Alcohol / Q000031:analogs & derivatives* / Q000494:pharmacology; D050050:Protein Carbonylation; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000139:chemically induced* / Q000473:pathology*; D014969:Xanthine Oxidase / Q000378:metabolism
chemical_list: D002109:Caffeic Acids; D009195:Peroxidase; D014969:Xanthine Oxidase; D003402:Creatine Kinase; D000243:Adenosine Deaminase; C055494:caffeic acid phenethyl ester; D010626:Phenylethyl Alcohol