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Today, similar observations have been made in AKI models of ischemia reperfusion injury (IRI).
Resveratrol, a dietary polyphenol with antioxidant and anti-inflammatory activity, has been shown to provide neuroprotection in models of ischemia.
In short-term animal models of ischemia, erythropoietin (EPO) signaling through the heterodimeric EPO receptor (EPOR)/β-common receptor (βCR) is believed to elicit tissue protective effects.
Administration of a myocardial protective gene (eg, heme oxygenase) via a recombinant adeno-associated virus vector reduces infarct size in animal models of ischemia and reperfusion.
Rosiglitazone (RSG), a PPAR-γ agonist, has been shown to reduce inflammation and provide neuroprotection in experimental models of ischemia and intracerebral hemorrhage.
Tc-99m-teboroxime demonstrates high myocardial extraction, an excellent flow to uptake relationship even at high flow rates [3], and differential clearance both in animal models of ischemia [4] [6] and in patients with ischemia [7] [10].
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Mast cell degranulation has been detected in models of ischemia-reperfusion models, but this mast cell activation might be a result of complement activation of mast cells [29].
The vasculoprotective property of HO-1 is evident in other experimental disease models of ischemia-reperfusion [22], atherogenesis [23] and vascular constriction [24].
Thus, animals treated with PARP-1 inhibitors or PARP-1 deficient mice showed decreased tissue damage and inflammatory mediators in several models of ischemia-reperfusion and heart transplantation (reviewed in [9]).
Given that resveratrol is known to be cardioprotective in models of ischemia-reperfusion [30], and our own findings of strong activity in the retardation of cardiac aging, but no effects on Pgc-1α transcriptional targets, it seems unlikely that SIRT1/Pgc-1α play a role in resveratrol's cardiac effects.
Sustained, enhanced non-oxidative glucose utilization has also been reported in models of ischemia-reperfusion [ 15].
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