GM1 stabilizes expression of NMDA receptor subunit 1 in the ischemic hemisphere of MCAo/reperfusion rat.
- Author:
Jian-ren LIU
1
;
Mei-ping DING
;
Er-qing WEI
;
Jian-hong LUO
;
Ying SONG
;
Jian-zheng HUANG
;
Qiu-fu GE
;
Hua HU
;
Li-jun ZHU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Brain Ischemia; metabolism; pathology; prevention & control; G(M1) Ganglioside; pharmacology; therapeutic use; Gene Expression Regulation; drug effects; Male; Middle Cerebral Artery; surgery; Neurons; drug effects; physiology; Protein Subunits; metabolism; Rats; Rats, Sprague-Dawley; Receptors, N-Methyl-D-Aspartate; metabolism; Reperfusion Injury; metabolism; pathology; prevention & control; Treatment Outcome
- From: Journal of Zhejiang University. Science. B 2005;6(4):254-258
- CountryChina
- Language:English
-
Abstract:
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).
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.
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).
CONCLUSIONGM1 can time-dependently reduce infarct volume in rats with focal cerebral I/R partly through stabilizing the expression of NMDAR1.