title: Electro-acupuncture preconditioning abrogates the elevation of c-Fos and c-Jun expression in neonatal hypoxic-ischemic rat brains induced by glibenclamide, an ATP-sensitive potassium channel blocker.
abstract: This study aimed to clarify the neuroprotective mechanism of electro-acupuncture (EA) preconditioning on hypoxic-ischemic brain injury (HIBI). Using Western blot, the expression of c-fos protein (c-Fos) and c-jun protein (c-Jun) induced by glibenclamide, an ATP-sensitive potassium (K(ATP)) channel blocker was examined from cerebral cortical and hippocampal samples in neonatal hypoxic-ischemic rats, with or without EA preconditioning. EA was performed on Hegu (LI4), a well-known acupoint commonly used in Oriental medicine for the treatment of neuronal injury resulting from hypoxia-ischemia (HI). Preconditioned rats were treated with either diazoxide, a K(ATP) channel opener, glibenclamide, or sterile saline injected into the left lateral ventricle (i.c.v.), with or without EA administration before HI insult. Interestingly, low c-Fos and c-Jun expressions were found both in diazoxide and EA groups, 24 h after HI. Furthermore, significant differences in relative optical density (ROD) were found between glibenclamide and HI control groups (P< or =0.05), as well as between the group administered glibenclamide after EA and the HI control group (P< or =0.05). However, the level of c-Fos and c-Jun expression in the group administered glibenclamide after EA was significantly lower than in the glibenclamide group (P< or =0.05). The present findings indicate that the effectiveness of EA preconditioning against HIBI may be mediated via the opening of K(ATP) channels.
authors.affiliation: Department of Neurology, Children's Hospital School of Medicine, Zhejiang University, 57 Zhugan Xiang, Hangzhou 310003, China. jiangkewen@21cn.com
authors.forename: Ke- Wen
authors.initials: K
authors.lastname: Jiang
authors.forename: Zheng- Yan
authors.initials: Z
authors.lastname: Zhao
authors.forename: Quan- Xiang
authors.initials: Q
authors.lastname: Shui
authors.forename: Zhe- Zhi
authors.initials: Z
authors.lastname: Xia
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D000959:Antihypertensive Agents / Q000494:pharmacology; D015153:Blotting, Western / Q000379:methods; D001921:Brain / Q000033:anatomy & histology / Q000187:drug effects*; D003981:Diazoxide / Q000494:pharmacology; D004195:Disease Models, Animal; D015671:Electroacupuncture; D005260:Female; D005905:Glyburide / Q000633:toxicity*; D020925:Hypoxia-Ischemia, Brain / Q000139:chemically induced / Q000378:metabolism / Q000628:therapy*; D008297:Male; D026902:Potassium Channel Blockers / Q000633:toxicity*; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D016755:Proto-Oncogene Proteins c-jun / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D000959:Antihypertensive Agents; D026902:Potassium Channel Blockers; D016760:Proto-Oncogene Proteins c-fos; D016755:Proto-Oncogene Proteins c-jun; D003981:Diazoxide; D005905:Glyburide