Ferreyra, CarlaVargas, FélixRodríguez-Gómez, IsabelPérez-Abud, RocíoO'Valle, FranciscoOsuna, Antonio2013-10-082013-10-082013-09-26Ferreyra C, Vargas F, Rodríguez-Gómez I, Pérez-Abud R, O'Valle F, Osuna A. Preconditioning with Triiodothyronine Improves the Clinical Signs and Acute Tubular Necrosis Induced by Ischemia/Reperfusion in Rats. PLoS ONE. 2013; 8(9):e74960http://hdl.handle.net/10668/1318JOURNAL ARTICLE;BACKGROUND Renal ischemia/reperfusion (I/R) injury is manifested by acute renal failure (ARF) and acute tubular necrosis (ATN). The aim of this study was to evaluate the effectiveness of preconditioning with 3, 3, 5 triiodothyronine (T3) to prevent I/R renal injury. METHODOLOGY/PRINCIPAL FINDINGS THE RATS WERE DIVIDED INTO FOUR GROUPS: sham-operated, placebo-treated (SO-P), sham-operated T3- treated (SO- T3), I/R-injured placebo-treated (IR-P), and I/R-injured T3-treated (IR- T3) groups. At 24 h before ischemia, the animals received a single dose of T3 (100 μg/kg). Renal function and plasma, urinary, and tissue variables were studied at 4, 24, and 48 h of reperfusion, including biochemical, oxidative stress, and inflammation variables, PARP-1 immunohistochemical expression, and ATN morphology. In comparison to the SO groups, the IR-P groups had higher plasma urea and creatinine levels and greater proteinuria (at all reperfusion times) and also showed: increased oxidative stress-related plasma, urinary, and tissue variables; higher plasma levels of IL6 (proinflammatory cytokine); increased glomerular and tubular nuclear PARP-1 expression; and a greater degree of ATN. The IR-T3 group showed a marked reduction in all of these variables, especially at 48 h of reperfusion. No significant differences were observed between SO-P and SO-T3 groups. CONCLUSIONS This study demonstrates that preconditioning rats with a single dose of T3 improves the clinical signs and ATN of renal I/R injury. These beneficial effects are accompanied by reductions in oxidative stress, inflammation, and renal PARP-1 expression, indicating that this sequence of factors plays an important role in the ATN induced by I/R injury.enAnimalesRatasTriyodotironinaNecrosis Tubular AgudaIsquemiaReperfusiónLesión Renal AgudaEstrés OxidativoPreacondicionamiento IsquémicoMedical Subject Headings::Organisms::Eukaryota::AnimalsMedical Subject Headings::Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::RatsMedical Subject Headings::Chemicals and Drugs::Hormones, Hormone Substitutes, and Hormone Antagonists::Hormones::Thyroid Hormones::Thyronines::TriiodothyronineMedical Subject Headings::Diseases::Male Urogenital Diseases::Urologic Diseases::Kidney Diseases::Renal Insufficiency::Acute Kidney Injury::Kidney Tubular Necrosis, AcuteMedical Subject Headings::Diseases::Pathological Conditions, Signs and Symptoms::Pathologic Processes::IschemiaMedical Subject Headings::Analytical, Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Perfusion::ReperfusionMedical Subject Headings::Diseases::Male Urogenital Diseases::Urologic Diseases::Kidney Diseases::Renal Insufficiency::Acute Kidney InjuryMedical Subject Headings::Phenomena and Processes::Physiological Phenomena::Physiological Processes::Stress, Physiological::Oxidative Stressresearch article24086411open access10.1371/journal.pone.00749601932-6203