The effects of the fibrin-derived peptide Bβ15-42 in acute and chronic rodent models of myocardial ischemia-reperfusion
Jazyk: | angličtina |
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Rok vydání: | 2007 |
Předmět: |
Male
Single drug dose Biomedical Research Myocardial Infarction Fibrin derivative Treatment response Animal tissue Mice Heart infarction size Models Acute heart infarction Treatment outcome Leukocyte migration Inbred BALB C CD18 Heart protection Ischemia-reperfusion Free Radical Scavengers Peptide derivative Reperfusion Injury Heart muscle ischemia Myocardial Reperfusion Preclinical study centers Article Scavenger Complement component C5 inhibitor Cyclic N-Oxides Animals Animal model Animal experiment Antigens Cytokine release Biology CD18 antigen Ischemic preconditioning Animal Interleukin-6 Myocardium Fibrinogen Tempol Nonhuman Biological Rats Drug effect Therapy effect Fibrin-derived peptide Disease Models Rat Heart muscle reperfusion Spin Labels Controlled study |
Popis: | Many compounds have been shown to prevent reperfusion injury in various animal models, although to date, translation into clinic has revealed several obstacles. Therefore, the National Heart, Lung, and Blood Institute convened a working group to discuss reasons for such failure. As a result, the concept of adequately powered, blinded, randomized studies for preclinical development of a compound has been urged. We investigated the effects of a fibrin-derived peptide Bβ15-42 in acute and chronic rodent models of ischemia-reperfusion at three different study centers (Universities of Dusseldorf and Vienna, TNO Biomedical Research). A total of 187 animals were used, and the peptide was compared with the free radical scavenger Tempol, CD18 antibody, α-C5 antibody, and the golden standard, ischemic preconditioning. We show that Bβ15-42 robustly and reproducibly reduced infarct size in all models of ischemia-reperfusion. Moreover, the peptide significantly reduced plasma levels of the cytokines interleukin 1β, tumor necrosis factor α, and interleukin 6. In rodents, Bβ15-42 inhibits proinflammatory cytokine release and is cardioprotective during ischemia-reperfusion injury. ©2007The Shock Society. |
Databáze: | OpenAIRE |
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