GM1 stabilizes expression of NMDA receptor subunit 1 in the ischemic hemisphere of MCAo/reperfusion rat

Objective: To determine the protective effect ofmonosialoganglionside (GM 1) and evaluate the influence ofGM 1 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...

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Published inJournal of Zhejiang University. B. Science Vol. 6; no. 4; pp. 254 - 258
Main Author 刘建仁 丁美萍 魏尔清 罗建红 宋英 黄鉴政 葛求富 胡华 朱丽君
Format Journal Article
LanguageEnglish
Published China Department of Neurology, Second Affiliated Hospital, School of Medicine,Zhejiang University, Hangzhou 310009, China%Department of Pharmacology,School of Medicine, Zhejiang University, Hangzhou 310009, China%Department of Neurobiology, School of Medicine, Zhejiang University, Hangzhou 310009, China%Department of Neurosurgery,Second Affiliated Hospital, School of Medicine,Zhejiang University, Hangzhou 310009, China 01.04.2005
Zhejiang University Press
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ISSN1673-1581
1862-1783
DOI10.1631/jzus.2005.B0254

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Abstract Objective: To determine the protective effect ofmonosialoganglionside (GM 1) and evaluate the influence ofGM 1 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, GM 1 ( 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 NMDAR 1 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 GM 1 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. GM 1 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: GM1 can time-dependently reduce infarct volume in rats with focal cerebral I/R partly through stabilizing the expression ofNMDAR1.
AbstractList To determine the protective effect of monosialoganglionside (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). 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. (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 min or 2 h after MCAo) was significantly higher than that of the control (P<0.05). GM1 can time-dependently reduce infarct volume in rats with focal cerebral I/R partly through stabilizing the expression of NMDAR1.
To determine the protective effect of monosialoganglionside (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).OBJECTIVETo determine the protective effect of monosialoganglionside (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).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.METHODSLeft 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.(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 min or 2 h after MCAo) was significantly higher than that of the control (P<0.05).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 min or 2 h after MCAo) was significantly higher than that of the control (P<0.05).GM1 can time-dependently reduce infarct volume in rats with focal cerebral I/R partly through stabilizing the expression of NMDAR1.CONCLUSIONGM1 can time-dependently reduce infarct volume in rats with focal cerebral I/R partly through stabilizing the expression of NMDAR1.
Objective: To determine the protective effect of monosialoganglionside (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 min or 2 h after MCAo) was significantly higher than that of the control (P<0.05). Conclusion: GM1 can time-dependently reduce infarct volume in rats with focal cerebral I/R partly through stabilizing the expression of NMDAR1.
Objective: To determine the protective effect ofmonosialoganglionside (GM 1) and evaluate the influence ofGM 1 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, GM 1 ( 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 NMDAR 1 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 GM 1 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. GM 1 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: GM1 can time-dependently reduce infarct volume in rats with focal cerebral I/R partly through stabilizing the expression ofNMDAR1.
Objective: To determine the protective effect of monosialoganglionside (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 min or 2 h after MCAo) was significantly higher than that of the control ( P <0.05). Conclusion: GM1 can time-dependently reduce infarct volume in rats with focal cerebral I/R partly through stabilizing the expression of NMDAR1.
R741; 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.
Author 刘建仁 丁美萍 魏尔清 罗建红 宋英 黄鉴政 葛求富 胡华 朱丽君
AuthorAffiliation DepartmentofNeurobiology,SchoolofMedicine,ZhejiangUniversity,Hangzhou310009,China DepartmentofNeurology,SecondAffiliatedHospital,SchoolofMedicine,ZhejiangUniversity,Hangzhou310009,China DepartmentofNeurosurgery,SecondAffiliatedHospital,SchoolofMedicine,ZhejiangUniversity,Hangzhou310009,China DepartmentofPharmacology,SchoolofMedicine,ZhejiangUniversity,Hangzhou310009,China
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Keywords G(M1) ganglioside
Rats
N-methyl-D-aspartate receptors
Reperfusion
Middle cerebral artery occlusion
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PublicationTitle Journal of Zhejiang University. B. Science
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PublicationYear 2005
Publisher Department of Neurology, Second Affiliated Hospital, School of Medicine,Zhejiang University, Hangzhou 310009, China%Department of Pharmacology,School of Medicine, Zhejiang University, Hangzhou 310009, China%Department of Neurobiology, School of Medicine, Zhejiang University, Hangzhou 310009, China%Department of Neurosurgery,Second Affiliated Hospital, School of Medicine,Zhejiang University, Hangzhou 310009, China
Zhejiang University Press
Publisher_xml – name: Department of Neurology, Second Affiliated Hospital, School of Medicine,Zhejiang University, Hangzhou 310009, China%Department of Pharmacology,School of Medicine, Zhejiang University, Hangzhou 310009, China%Department of Neurobiology, School of Medicine, Zhejiang University, Hangzhou 310009, China%Department of Neurosurgery,Second Affiliated Hospital, School of Medicine,Zhejiang University, Hangzhou 310009, China
– name: Zhejiang University Press
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References_xml – reference: 8487863 - Nature. 1993 May 20;363(6426):260-3
– reference: 1967639 - J Neurosci. 1990 Jan;10(1):283-92
– reference: 9016349 - Mol Pharmacol. 1997 Jan;51(1):79-86
– reference: 1970230 - Annu Rev Neurosci. 1990;13:171-82
– reference: 8474009 - J Pharmacol Exp Ther. 1993 Apr;265(1):24-9
– reference: 2167544 - Trends Pharmacol Sci. 1990 Jul;11(7):290-6
– reference: 8861717 - Brain Res Dev Brain Res. 1996 Mar 29;92(1):10-7
– reference: 12626876 - J Neurocytol. 2001 Dec;30(12):945-55
– reference: 11165369 - Brain Res Mol Brain Res. 2001 Jan 31;86(1-2):34-47
– reference: 10659851 - Nature. 2000 Jan 20;403(6767):316-21
– reference: 14653951 - Acta Pharmacol Sin. 2003 Dec;24(12):1241-7
– reference: 9742162 - J Neurosci. 1998 Oct 1;18(19):7953-61
– reference: 11248442 - Neurosci Lett. 2001 Mar 30;301(2):139-42
– reference: 2543272 - Annu Rev Pharmacol Toxicol. 1989;29:365-402
– reference: 2643202 - Stroke. 1989 Jan;20(1):84-91
– reference: 1688945 - J Pharmacol Exp Ther. 1990 Jan;252(1):419-27
– reference: 2236016 - Proc Natl Acad Sci U S A. 1990 Oct;87(20):8017-21
– reference: 8313938 - Exp Neurol. 1994 Feb;125(2):195-217
– reference: 12065629 - J Neurochem. 2002 May;81(4):696-707
– reference: 8501519 - J Neurosci. 1993 Jun;13(6):2483-94
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Snippet Objective: To determine the protective effect ofmonosialoganglionside (GM 1) and evaluate the influence ofGM 1 on expression of N-methyl-D-aspartate receptor...
To determine the protective effect of monosialoganglionside (GM1) and evaluate the influence of GM1 on expression of N-methyl-D-aspartate receptor subunit 1...
Objective: To determine the protective effect of monosialoganglionside (GM1) and evaluate the influence of GM1 on expression of N-methyl-D-aspartate receptor...
R741; Objective: To determine the protective effect ofmonosialoganglionside (GM1) and evaluate the influence of GM1 on expression of N-methyl-D-aspartate...
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SubjectTerms Animals
Biomedicine
Brain Ischemia - metabolism
Brain Ischemia - pathology
Brain Ischemia - prevention & control
G(M1) Ganglioside - pharmacology
G(M1) Ganglioside - therapeutic use
Gene Expression Regulation - drug effects
Male
Middle Cerebral Artery - surgery
Neurons - drug effects
Neurons - physiology
Protein Subunits - metabolism
Rats
Rats, Sprague-Dawley
Receptors, N-Methyl-D-Aspartate - metabolism
Reperfusion Injury - metabolism
Reperfusion Injury - pathology
Reperfusion Injury - prevention & control
Treatment Outcome
再灌注
冬氨酸盐
神经节苷脂
脑动脉栓塞
Title GM1 stabilizes expression of NMDA receptor subunit 1 in the ischemic hemisphere of MCAo/reperfusion rat
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https://www.ncbi.nlm.nih.gov/pubmed/15754422
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https://pubmed.ncbi.nlm.nih.gov/PMC1389733
Volume 6
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