title: Protective effect of caffeine administration on myocardial ischemia/reperfusion injury in rats.
abstract: Many studies have examined the association between coffee consumption and risk of cardiovascular disease, but the results remain controversial. Caffeine is one of the main biologically active compounds of coffee. The aim of this study was to investigate the potential role of caffeine on myocardial ischemia/reperfusion (I/R) injury in the rats. We administered caffeine (25 mg/kg per day) or saline in rats for 4 weeks before myocardial ischemia/reperfusion operation. Compared with the sham group, caffeine treatment decreased ischemia-associated infarct size, serum creatine kinase, and lactate dehydrogenase 3-h reperfusion after 30-min ischemia. Myocardial neutrophil infiltration (assessed by myeloperoxidase activity) was significantly decreased compared with the control group. Meanwhile, caffeine reduced the myocardial apoptosis and suppressed the activation of caspase 3 during myocardial I/R. Importantly, we observed a strong poly(ADP-ribose) polymerase (PARP) activation during myocardial I/R, and caffeine administration inhibited PARP activation and attenuated the expression of PARP-related proinflammatory mediators such as inducible nitric oxide synthetase, IL-6, and TNF-α, all of which may be correlated with downregulated nuclear factor κB activity. We concluded that caffeine protected against myocardial I/R injury by inhibiting inflammation and apoptosis.
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, People's Republic of China.
authors.forename: Xu-Yong
authors.initials: XY
authors.lastname: Li
authors.forename: Lin
authors.initials: L
authors.lastname: Xu
authors.forename: Guo-Sheng
authors.initials: GS
authors.lastname: Lin
authors.forename: Xiao-Yan
authors.initials: XY
authors.lastname: Li
authors.forename: Xue-Jun
authors.initials: XJ
authors.lastname: Jiang
authors.forename: Tao
authors.initials: T
authors.lastname: Wang
authors.forename: Jing-Jun
authors.initials: JJ
authors.lastname: Lü
authors.forename: Bin
authors.initials: B
authors.lastname: Zeng
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D002110:Caffeine / Q000627:therapeutic use*; D053148:Caspase 3 / Q000378:metabolism; D003402:Creatine Kinase / Q000097:blood; D024202:Electrophoretic Mobility Shift Assay; D006836:Hydro-Lyases / Q000097:blood; D007150:Immunohistochemistry; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D016328:NF-kappa B / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015850:Interleukin-6; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D002110:Caffeine; D052247:Nitric Oxide Synthase Type II; D003402:Creatine Kinase; D053148:Caspase 3; D006836:Hydro-Lyases; C045581:lactate dehydratase