L. Xu and H. Sun Pages 1188 - 1193 ( 6 )
Brain ischemia resulting from multiple disease states including cardiac arrest, stroke and traumatic brain injury, is a leading cause of death and disability. Despite significant resources dedicated to developing pharmacological interventions, few effective therapeutic options are currently available. The basic consequence of cerebral ischemia, characterized by energy failure and subsequent brain metabolic abnormalities, enables the protective effects by pharmacological manipulation of brain metabolism. We present here the important roles of brain glycogen metabolism and propose inhibition of glycogenolysis as a therapeutic approach to cerebral ischemia.
Brain glycogen, cerebral ischemia, glycogenolysis, inhibitors, Brain ischemia, traumatic brain injury, brain glycogen metabolism, Brain, Neurons, glycogen synthase, Astrocytes, neurotransmitters, glycogen phosphorylase, phosphorylase kinase, glucose-6-phosphate, hypoglycemia, oxidative phosphorylation, glutamate mediated excitotox-icity, Glycogen Storage, methinionine sulfoximine, glucose-depleted brain tissue, glutathione system, Glutathione disulfide, Amelioration of Lactic Acidosis, glycolytic pathway, glycolytic substrate, Mitochondria, reactive oxygen species, Maslinic Acid, CP-316819, Magnesium Sulfate, N-methyl-D-aspartate, Uridine diphosphate glucose, uridine triphos-phate, glucose-1-phosphate uridyltrans-ferase, electroencephalogram
Center for Drug Discovery, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing 210009, China.