| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5845987 | Toxicology and Applied Pharmacology | 2015 | 11 Pages |
Abstract
IO did not impair the capacity of DOX to decrease cancer cell viability and could even prevent some aspects of DOX cardiotoxicity in cardiomyocytes and in mice.
Keywords
RT-PCRLVEFIVSIVRTBNPLVEDdIVCTi.p.LVESDiNOSβ-MHCANPmRNAESRLVPWDOXIsovolumic contraction timestandard error of the mean.cDNAcomplementary deoxyribonucleic acidelectrocardiogramECGischemia/reperfusionOxidative stressCell proliferationintra peritonealDoxorubicinleft ventricular posterior wallElectron spin resonancemessenger ribonucleic acidRONSIsovolumic relaxation timebeta-myosin heavy chainCardiotoxicityinducible nitric oxide synthaseleft ventricular end-diastolic diameterleft ventricular end-systolic diameterSEMIron overloadArbitrary Unitreverse transcription polymerase chain reactionbrain natriuretic peptideatrial natriuretic peptideleft ventricular ejection fractionReactive oxygen and nitrogen species
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Authors
Charles Guenancia, Na Li, Olivier Hachet, Eve Rigal, Yves Cottin, Patrick Dutartre, Luc Rochette, Catherine Vergely,