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The protection conferred against ischemia-reperfusion injury in the diabetic brain by N-acetylcysteine is associated with decreased dicarbonyl stress.
Abstract Diabetes, a risk factor for stroke, leads to elevated blood methylglyoxal (MG) levels. This is due to increased MG generation from the high glucose levels, and because diabetes impairs the glutathione (GSH)-glyoxalase system for MG elimination. MG glycates proteins and causes dicarbonyl stress. We investigated the contribution of MG and GSH to stroke outcome. Cerebral ischemia/reperfusion was performed in chemical-induced (streptozotocin) and genetic Akita mouse models of Type 1 diabetes. Brain infarction and functions of the GSH-dependent MG elimination pathway were determined. Diabetes increased post-is...
Source: Free Radical Biology and Medicine - April 11, 2016 Category: Biology Authors: Wang B, Yee Aw T, Stokes KY Tags: Free Radic Biol Med Source Type: research

Hypoxia-inducible factor 1 contributes to N-acetylcysteine's protection in stroke.
Abstract Stroke is a leading cause of adult morbidity and mortality with very limited treatment options. Evidence from pre-clinical models of ischemic stroke has demonstrated that the antioxidant N-acetylcysteine (NAC) effectively protects the brain from ischemic injury. Here, we evaluated a new pathway through which NAC exerted its neuroprotection in a transient cerebral ischemia animal model. Our results demonstrated that pre-treatment of NAC increased protein levels of hypoxia-inducible factor-1α (HIF-1α), the regulatable subunit of HIF-1, and its target proteins erythropoietin (EPO) and glucose transporter (...
Source: Free Radical Biology and Medicine - November 29, 2013 Category: Biology Authors: Zhang Z, Yan J, Taheri S, Liu J, Shi H Tags: Free Radic Biol Med Source Type: research