Gap junction communication involved in brain protection following focal ischemia and reperfusion in rats

doi:10.3969/j.issn.1673-5374.2009.09.007

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	Gap junction communication involved in brain protection following focal ischemia and reperfusion in rats
	Wang, F; Hai, J; Jing, YH; Jing, YH (reprint author), Lanzhou Univ, Sch Basic Med Sci, Lanzhou 730000, Gansu, Peoples R China.
刊名	NEURAL REGENERATION RESEARCH
	2009-09
卷号	4 期号:9 页码:677-682
关键词	gap junction brain ischemia astrocytes microglia rats
ISSN号	1673-5374
DOI	10.3969/j.issn.1673-5374.2009.09.007
文献子类	Article
英文摘要	BACKGROUND: Studies have suggested that gap junctions not only modulate the fate of the neocortex, but are also involved in maintaining homeostasis in the mature brain. However, the neuroprotective effects of gap junction communication following brain ischemic injury remain poorly understood. OBJECTIVE: To investigate the neuroprotective effects and possible mechanisms of gap junction communication following focal ischemia and reperfusion. DESIGN, TIME AND SETTING: A randomized, controlled, animal experiment was performed at the School of Basic Medical Sciences of Lanzhou University between June 2007 and May 2008. MATERIALS: Rabbit polyclonal anti-connexin 43 (Cx43) and gap junction blocking agent octanol were purchased from Sigma, USA; mouse monoclonal anti-rat glial fibrillary acidic protein (GFAP) was provided by Santa Cruz, USA; mouse monoclonal anti-rat CD11b was produced by Abcam, England. METHODS: A total of 52 adult, male, Sprague Dawley rats were randomly assigned to three groups: sham-operated (n = 12), vehicle control (n = 20), and octanol-treated (n = 20). Brain ischemia and reperfusion were induced by transient middle cerebral artery occlusion (MCAC) in vehicle control and octanol-treated groups, while no MCAO was administered to the sham-operated group. In the octanol-treated group, 5 mmol/kg octanol was dissolved in dimethyl sulfoxide (0.005% V/V) and was intraperitoneally injected 30 minutes prior to ischemic onset. Sham-operated and vehicle groups received equivalent volumes of dimethyl sulfoxide. MAIN OUTCOME MEASURES: Infarct volumes in ipsilateral striaturn after MCAO were measured using cresyl violet dye; GFAP, CD11 b, and Cx43 expression in the ipsilateral striaturn following MCAO were detected by immunohistochemistry; Western blot analysis was employed to determine Cx43 and GFAP expression. RESULTS: At 1 and 3 days following MCAO and reperfusion, ipsilateral striaturn infarct volumes in the octanol group were significantly greater than in the vehicle group (P < 0.05). There was no infarction in the sham-operated group. Cx43 and GFAP expression in the ipsilateral striaturn of the octanol group was remarkably decreased compared with the vehicle group (P < 0.05), and expression in the sham-operated group was less than in the other two groups (P < 0.05). In the octanol-treated group, CD11b expression was significantly increased compared with the vehicle group (P < 0.05), and there were less CD11b-immunoreactive cells in the sham-operated group compared with the other two groups (P < 0.05). CONCLUSION: The pretreatment of blocking gap junction aggravated brain injury following MCAC. These results were possibly due to reduced astrocyte proliferation and activation, as well as reduced inflammatory response via activated microglia.
学科主题	Cell Biology ; Neurosciences & Neurology
出版地	SHENYANG
语种	英语
CSCD记录号	CSCD:3680684
WOS记录号	WOS:000270690300007
内容类型	期刊论文
源URL	[http://ir.lzu.edu.cn/handle/262010/121423]
专题	基础医学院_期刊论文
通讯作者	Jing, YH (reprint author), Lanzhou Univ, Sch Basic Med Sci, Lanzhou 730000, Gansu, Peoples R China.
推荐引用方式 GB/T 7714	Wang, F,Hai, J,Jing, YH,et al. Gap junction communication involved in brain protection following focal ischemia and reperfusion in rats[J]. NEURAL REGENERATION RESEARCH,2009,4(9):677-682.
APA	Wang, F,Hai, J,Jing, YH,&Jing, YH .(2009).Gap junction communication involved in brain protection following focal ischemia and reperfusion in rats.NEURAL REGENERATION RESEARCH,4(9),677-682.
MLA	Wang, F,et al."Gap junction communication involved in brain protection following focal ischemia and reperfusion in rats".NEURAL REGENERATION RESEARCH 4.9(2009):677-682.