Glycation abolishes the cardioprotective effects of albumin during ex vivo ischemia-reperfusion

dc.contributor.authorMapanga, Rudo F.en_ZA
dc.contributor.authorJoseph, Danzil E.en_ZA
dc.contributor.authorSaieva, Marcoen_ZA
dc.contributor.authorBoyer, Florenceen_ZA
dc.contributor.authorRondeau, Philippeen_ZA
dc.contributor.authorBourdon, Emmanuelen_ZA
dc.contributor.authorEssop, M. Faadielen_ZA
dc.date.accessioned2019-02-22T06:37:06Z
dc.date.available2019-02-22T06:37:06Z
dc.date.issued2017
dc.descriptionCITATION: Mapanga, R. F., et al. 2017. Glycation abolishes the cardioprotective effects of albumin during ex vivo ischemia-reperfusion. Physiological Reports, 5(2):e13107, doi:10.14814/phy2.13107.
dc.descriptionThe original publication is available at https://physoc.onlinelibrary.wiley.com/journal/2051817x
dc.description.abstractHyperglycemia‐induced oxidative stress plays a key role in the onset/progression of cardiovascular diseases. For example, it can trigger formation of advanced glycation end (AGE) products with ischemia‐reperfusion performed under hyperglycemic conditions. For this study, we hypothesized that albumin modified by glycation loses its unique cardioprotective properties in the setting of ischemia‐reperfusion under high glucose conditions. Here, ex vivo rat heart perfusions were performed under simulated normo‐ and hyperglycemic conditions, that is Krebs‐Henseleit buffer containing 11 mmol/L and 33 mmol/L glucose, respectively, ± normal or glycated albumin preparations. The perfusion protocol consisted of a 60 min stabilization step that was followed by 20 min of global ischemia and 60 min reperfusion. Additional experiments were completed to determine infarct sizes in response to 20 min regional ischemia and 120 min reperfusion. At the end of perfusions, heart tissues were isolated and evaluated for activation of the AGE pathway, oxidative stress, and apoptosis. Our data reveal that native bovine serum albumin treatment elicited cardioprotection (improved functional recovery, decreased infarct sizes) under high glucose conditions together with enhanced myocardial antioxidant capacity. However, such protective features are lost with glycation where hearts displayed increased infarct sizes and poor functional recovery versus native albumin treatments. Myocardial antioxidant capacity was also lowered together with activation of the intracellular AGE pathway. These data therefore show that although albumin acts as a cardioprotective agent during ischemia‐reperfusion, it loses its cardioprotective and antioxidant properties when modified by glycation.en_ZA
dc.description.urihttps://physoc.onlinelibrary.wiley.com/doi/full/10.14814/phy2.13107
dc.description.versionPublisher's version
dc.format.extent10 pages
dc.identifier.citationMapanga, R. F., et al. 2017., Glycation abolishes the cardioprotective effects of albumin during ex vivo ischemia-reperfusion. Physiological Reports, 5(2):e13107, doi:10.14814/phy2.13107
dc.identifier.issn2051-817X (online)
dc.identifier.otherdoi:10.14814/phy2.13107
dc.identifier.urihttp://hdl.handle.net/10019.1/105458
dc.language.isoen_ZAen_ZA
dc.publisherWiley Open Access
dc.rights.holderAuthors retain copyright
dc.subjectAlbuminsen_ZA
dc.subjectCardiovascular system--Diseasesen_ZA
dc.subjectHyperglycemiaen_ZA
dc.subjectGlycosylationen_ZA
dc.subjectReperfusion injuryen_ZA
dc.subjectOxidative stressen_ZA
dc.titleGlycation abolishes the cardioprotective effects of albumin during ex vivo ischemia-reperfusionen_ZA
dc.typeArticleen_ZA
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