Recombinant human erythropoietin (rhEPO) preconditioning on nuclear factor-kappa B (NF-kB) activation & proinflammatory cytokines induced by myocardial ischaemia-reperfusion.

dc.contributor.authorLiu, Xiaomingen_US
dc.contributor.authorShen, Jinchunen_US
dc.contributor.authorJin, Yien_US
dc.contributor.authorDuan, Manlinen_US
dc.contributor.authorXu, Jianguoen_US
dc.date.accessioned2006-09-07en_US
dc.date.accessioned2009-05-27T08:31:21Z
dc.date.available2006-09-07en_US
dc.date.available2009-05-27T08:31:21Z
dc.date.issued2006-09-07en_US
dc.description.abstractBACKGROUND & OBJECTIVES: Erythropoietin (EPO), originally identified for its critical hormonal role in promoting erythrocyte survival and differentiation, has shown to a protective effect in myocardial ischaemia-reperfusion (I-R) injury in animal model. However, the precise mechanisms remain unclear. The objective of this study was to determine the roles of nuclear factor-kappa B (NF-kB) and associated cytokines induced by I-R in the cardioprotection by recombinant human erythropoietin (rhEPO). Morphopathological observations were also made on the ultrastructure of myocardial tissue. METHODS: Myocardial I-R rat model was established by 30 min ligation of left descending coronary and 3 h reperfusion. RhEPO or saline solution was intraperitoneally injected 24 h before I-R insult. The infarct sizes were measured by triphenyltetrazolium chloride (TTC)-Evans blue technique and ultrastructural organizations were observed by a transmission electron microscope. Tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and IL-10 concentrations were analyzed by enzyme-linked immunosorbance assays and NF-kB by electrophoretic mobility shift assay. TNF-alpha and IL-6 mRNA expression were studied by the reverse-transcription polymerase chain reaction (RT-PCR). RESULTS: A single bolus injection of 5,000 units/kg of rhEPO 24 h before insult remarkably reduced infarct size and improved ultrastructural organization of I-R myocardium. It greatly suppressed TNF-alpha and IL-6 expression, but enhanced IL-10 production. It modestly activated NF-kB before I-R insult and markedly attenuated subsequent NF-kB activation during sustained I-R. INTERPRETATION & CONCLUSION: The suppression of proinflammatory cytokines expression may act by inhibiting NF-kB activation during I-R, but not by induction of IL-10. This might be one of the molecular mechanisms of rhEPO in cardioprotection. In addition, NF-kB was suggested to play a dual role in cardioprotective effects of rhEPO.en_US
dc.description.affiliationDepartment of Anaesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.en_US
dc.identifier.citationLiu X, Shen J, Jin Y, Duan M, Xu J. Recombinant human erythropoietin (rhEPO) preconditioning on nuclear factor-kappa B (NF-kB) activation & proinflammatory cytokines induced by myocardial ischaemia-reperfusion. Indian Journal of Medical Research. 2006 Sep; 124(3): 343-54en_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/24741
dc.language.isoengen_US
dc.source.urihttps://icmr.nic.in/ijmr/ijmr.htmen_US
dc.subject.meshAnalysis of Varianceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCytokines --metabolismen_US
dc.subject.meshDNA Primersen_US
dc.subject.meshElectrophoretic Mobility Shift Assayen_US
dc.subject.meshEnzyme-Linked Immunosorbent Assayen_US
dc.subject.meshErythropoietin, Recombinant --metabolismen_US
dc.subject.meshIschemic Preconditioning, Myocardial --methodsen_US
dc.subject.meshMaleen_US
dc.subject.meshMicroscopy, Electron, Transmissionen_US
dc.subject.meshMyocardial Reperfusion Injury --metabolismen_US
dc.subject.meshMyocardium --ultrastructureen_US
dc.subject.meshNF-kappa B --metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.titleRecombinant human erythropoietin (rhEPO) preconditioning on nuclear factor-kappa B (NF-kB) activation & proinflammatory cytokines induced by myocardial ischaemia-reperfusion.en_US
dc.typeComparative Studyen_US
dc.typeJournal Articleen_US
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