Glutamate dehydrogenase as a neuroprotective target against brain ischemia and reperfusion

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• 作者：A Young Kim^a ; ^b ; Kyeong-Hoon Jeong^c ; Jae Ho Lee^d ; Yup Kang^b ; Soo Hwan Lee^a ; Eun Joo Baik^a ; ^b ; ^{eunjoo@ajou.ac.kr}
• 关键词：AAT ; aspartate aminotransferase ; GAPDH ; glyceraldehyde-3-phosphate dehydrogenase ; GDH ; glutamate dehydrogenase ; I/R ; ischemia and reperfusion ; IOA ; iodoacetate ; OGD ; oxygen and glucose deprivation ; TCA ; tricarboxylic acid ; α-KG ; alpha-ketoglutarate ; EDTA ; ethylenediaminetetraacetic acid ; EGTA ; ethylene glycol tetraacetic acid ; HEPES ; 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid ; PBS ; phosphate-buffered saline ; FBS ; fetal bovine serum ; Ara-C ; cytosine arabinofuranoside ; PMSF ; phenylmethylsu
• 刊名：Neuroscience
• 出版年：2017
• 出版时间：6 January 2017
• 年：2017
• 卷：340
• 期：Complete
• 页码：487-500
• 全文大小：2189 K
• 卷排序：340

文摘

In brain ischemia and reperfusion, α-ketoglutarate and ATP were severely depleted. Glutamate dehydrogenase catalyzes glutamate into α-ketoglutarate, finally producing intracellular ATP. Beta-lapachone stimulated the activation of mitochondrial glutamate dehydrogenase in energy-depleted conditions. Beta-lapachone provided glutamate dehydrogenase-mediated influx of α-ketoglutarate into the TCA cycle and production of ATP. Thus, the activation of glutamate dehydrogenase by BCH and beta-lapachone represents a potential neuroprotective strategy.