| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10958140 | Neurochemistry International | 2012 | 10 Pages |
Abstract
⺠Glycine could attenuate ischemia/reperfusion (I/R) induced cerebral infarction and improved neurological outcomes in mice. ⺠Glycine effectively inhibits transient brain I/R-induced neuronal apoptosis. ⺠The mechanism may be via suppressing the “intrinsic” and the “extrinsic” apoptotic pathways. ⺠The protective effect of glycine against I/R injury to neurons may be mediated by GlyR rather than NMDA receptor.
Keywords
OGDterminal deoxynucleotidyl transferase biotin-dUTP nick end labelingGlyRs3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyltetrazolium bromideMCAON-methyl-d-aspartateNMDATTCIACUCJnk2,3,5-triphenyl tetrazolium chloridec-Jun N-terminal kinaseERK1/2I/RMTTsiRNAmiddle cerebral artery occlusionischemia/reperfusioncerebral ischemia/reperfusionTUNELApoptosisCNSInstitutional Animal Care and Use CommitteeSH-SY5Y cellcentral nervous systemlactate dehydrogenaseLDHOxygen and glucose deprivationNeuronsextracellular signal-regulated kinase 1 and 2GlycineGlycine receptorsglycine receptor
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Authors
Yan Lu, Jing Zhang, Bingqing Ma, Kexue Li, Xiaoyu Li, Hui Bai, Qing Yang, Xudong Zhu, Jingjing Ben, Qi Chen,