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GM1 stabilizes expression of NMDA receptor subunit 1 in the ischemic hemisphere of MCAo/reperfusion rat
作者姓名:Liu JR  Ding MP  Wei EQ  Luo JH  Song Y  Huang JZ  Ge QF  Hu H  Zhu LJ
作者单位:Department of Neurology,Department of Neurology,Department of Pharmacology,Department of Neurobiology,School of Medicine,Zhejiang University,Hangzhou 310009,China,Department of Pharmacology,Department of Neurology,Department of Pharmacology,Department of Neurosurgery,Second Affiliated Hospital,School of Medicine,Zhejiang University,Hangzhou 310009,China,Department of Neurobiology,School of Medicine,Zhejiang University,Hangzhou 310009,China
基金项目:浙江省卫生厅资助项目,国家重点基础研究发展计划(973计划),国家自然科学基金
摘    要:INTRODUCTION GM1 ganglioside (GM1) is the main kind ofgangliosides in mammalia, and most abundant inbrain tissue (Duchemin et al., 2002). It was reportedthat GM1 could protect cerebral ischemia in vivo andin vitro, one protective mechanism of which is thatGM1 could reduce neural injury induced by toxicityof excitatory amino acid via N-methyl-D-aspartate receptor (NMDAR) (Kharlamov et al., 1993; Simon et al., 1993; Garofalo and Cue…

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收稿时间:20 November 2008

GM1 stabilizes expression of NMDA receptor subunit 1 in the ischemic hemisphere of MCAo/reperfusion rat
Liu JR,Ding MP,Wei EQ,Luo JH,Song Y,Huang JZ,Ge QF,Hu H,Zhu LJ.GM1 stabilizes expression of NMDA receptor subunit 1 in the ischemic hemisphere of MCAo/reperfusion rat[J].Journal of Zhejiang University Science,2005,6(4):254-258.
Authors:Liu Jian-ren  Ding Mei-ping  Wei Er-qing  Luo Jian-hong  Song Ying  Huang Jian-zheng  Ge Qiu-fu  Hu Hua  Zhu Li-jun
Institution:Department of Neurology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China. Liujianren@medmail.com.cn
Abstract:Objective: To determine the protective effect ofmonosialoganglionside (GM1) and evaluate the influence of GM1 on expression of N-methyl-D-aspartate receptor subunit 1 (NMDAR1) in Sprague-Dawley (SD) rats with focal cerebral ischemia-reperfusion (I/R). Methods: Left middle cerebral artery (MCA) was occluded by an intraluminal suture for 1 h and the brain was reperfused for 72 h in SD rats when infarct volume was measured, GM1 (10 mg/kg) was given ip (intraperitoneally) at 5 min(group A), 1 h (group B) and 2 h (group C) after MCA occlusion (MCAo). Expression of NMDAR1 was detected by Western blot at various time after reperfusion (4 h, 6 h, 24 h, 48 h and 72 h) in ischemic hemispheres of the rats with or without GM1 administered. Results: (1) Adjusted relative infarct volumes of groups A and B were significantly smaller than that of group C and the control group (P<0.01 and P<0.05, respectively). (2) Expression level of NMDAR1 was temporally high at 6 h after reperfusion,and dipped below the normal level at 72 h after reperfusion. GM1 at 5 min after MCAo significantly suppressed the expression of NMDAR1 at 6 h after reperfusion (P<0.05 vs the control). At 72 h after reperfusion, the NMDAR1 expression level of rats treated with GM1 administered (at 5 rain or 2 h after MCAo) was significantly higher than that of the control (P<0.05). Conclusion: GM1can time-dependently reduce infarct volume in rats with focal cerebral I/R partly through stabilizing the expression ofNMDAR1.
Keywords:G(M1) ganglioside  Middle cerebral artery occlusion  Reperfusion  N-methyl-D-aspartate receptors  Rats
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