title: Electroacupuncture regulates NMDA receptor NR1 subunit expression via PI3-K pathway in a rat model of cerebral ischemia-reperfusion.
abstract: Cell survival is regulated by the balance between death and survival signals. Previous studies have shown that the N-methyl-d-aspartate receptors (NMDARs) are responsible for the glutamate-induced excitotoxicity in the postischemic brain. Meanwhile, nerve growth factor (NGF) is critically involved in cell survival and neuroprotective effects via the extracellular signal-related kinase (ERK) pathway or the phosphatidylinositol 3-kinase (PI3-K) pathway mediated by the high affinity NGF receptor, tropomyosin-related kinase A (TrkA). Clinically, electroacupuncture (EA) has been shown to produce beneficial effects on stroke patients. However, the detailed mechanisms mediating the beneficial effects of EA on stroke are still unknown. In the present study, we found that EA treatment reversed the high expression of NR1 subunit and up-regulated the level of TrkA in a rat model of middle cerebral artery occlusion. Using protein kinase inhibitors of specific intracellular signaling pathways, we found that the neuroprotective effects of EA appear to be mediated by stimulation of the PI3-K pathway, but not ERK pathway. These findings may provide important experimental evidence for the clinical application of EA treatment for stroke patients.
authors.affiliation: Department of Neurobiology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, P.R. China.
authors.forename: Ning
authors.initials: N
authors.lastname: Sun
authors.forename: Xiaojing
authors.initials: X
authors.lastname: Zou
authors.forename: Jing
authors.initials: J
authors.lastname: Shi
authors.forename: Xiaochun
authors.initials: X
authors.lastname: Liu
authors.forename: Lingli
authors.initials: L
authors.lastname: Li
authors.forename: Li
authors.initials: L
authors.lastname: Zhao
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D015671:Electroacupuncture; D020244:Infarction, Middle Cerebral Artery / Q000150:complications / Q000201:enzymology / Q000628:therapy; D002546:Ischemic Attack, Transient / Q000150:complications / Q000201:enzymology* / Q000517:prevention & control; D008297:Male; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D021122:Protein Subunits / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D020917:Receptor, trkA / Q000235:genetics / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000235:genetics / Q000378:metabolism*; D015427:Reperfusion Injury / Q000150:complications / Q000201:enzymology* / Q000517:prevention & control; D015398:Signal Transduction / Q000502:physiology
chemical_list: C409466:NR1 NMDA receptor; D021122:Protein Subunits; D012333:RNA, Messenger; D016194:Receptors, N-Methyl-D-Aspartate; D019869:Phosphatidylinositol 3-Kinases; D020917:Receptor, trkA