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  • infarct size
  • Next, we found that naringin was able to cross the blood-brain barrier, and naringin decreased neurological deficit score, reduced infarct size, and attenuated apoptotic cell death in the ischemia-reperfused rat brains. (springer.com)
  • Mice
  • The study, published today in the OnlineFirst version of the Journal of Parenteral and Enteral Nutrition ( JPEN ), the research journal of the American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.), used a mice model to compare the effects of GLN on hind limb ischemia reperfusion (IR) injury. (nutritioncare.org)
  • The study subjected three groups of mice to 90 minutes of ischemia followed by a variable period of reperfusion. (nutritioncare.org)
  • inflammation
  • We therefore hypothesize that administration of human AM/AMBP-1, even after reperfusion, improves cardiovascular function, attenuates organ injury and inflammation responses, and reduces mortality following gut I/R injury. (sbir.gov)
  • When the organ is ready for the transplantation, the reperfusion of the organ induces an increase of the oxidative stress, endoplasmic reticulum stress, and inflammation which causes tissue damage, resulting in a decrease of the transplantation success. (mdpi.com)
  • Inflammation is a subsequent event of spinal cord ischemia and possibly a major contributor to spinal cord IRI. (hindawi.com)
  • necrosis
  • A-769662 also augmented endothelial nitric oxide synthase (eNOS) activation during ischemia, which partially attenuated myocardial stunning, but did not prevent necrosis. (nih.gov)
  • organs
  • The storage of organs in preservation solutions is followed by the ischemia of the organ, resulting in a shortage of oxygen and nutrients, which damage the tissues. (mdpi.com)
  • The goal of this review is to summarize the role of the proteasome and pharmacological compounds that regulate the proteasome in protecting the organs from the ischemia-reperfusion injury. (mdpi.com)
  • The use of AMPK activators may represent a novel strategy to protect the heart and other solid organs against ischemia. (nih.gov)
  • protective
  • Although we have shown that administration of rat AM plus human AMBP-1 at the beginning of reperfusion is protective, it remains unknown whether a combination of human AM and human AMBP-1 is also beneficial and, if so, whether delayed administration of AM/AMBP-1 (which is more clinically relevant) reduces gut I/R-induced mortality. (sbir.gov)
  • C57Bl
  • C) Isolated C57Bl/6 hearts were treated with A-769662 (100 μmol/L) or vehicle for 30 min prior to global no-flow ischemia (25 min) and reperfusion (30 min). (nih.gov)
  • subsequent
  • Isolated AMPK inactivated kinase dead (KD) hearts were treated with A-769662 (100 μmol/L) or vehicle for 30 min during baseline aerobic perfusion, prior to global no-flow ischemia (25 min) and subsequent reperfusion (30 min) without compound. (nih.gov)
  • cellular
  • In particular, ischemia leads to depletion of cellular energy, accumulation of intracellular sodium, calcium, and reactive oxygen species (ROS), and activation of multiple enzyme systems leading to cell damage [ 3 ]. (hindawi.com)
  • minutes
  • Blood samples were drawn from all animals to evaluate plasma neutrophil gelatinase-associated lipocalin (NGAL) at the beginning, 15 minutes after ischemia, 15 minutes after reperfusion, and 6 hours after the surgical procedure (T0, T1, T2, and T3, respectively). (dovepress.com)