Effect of Ginsenoside Rd Pretreatment on the Expressions of NR2B Receptor and Endonuclease G After Focal Cerebral Ischemia-Reperfusion in Rats
- VernacularTitle:人参皂苷Rd预处理对局灶性脑缺血再灌注大鼠NR2B受体和核酸内切酶G表达的影响
- Author:
Xuhui DU
;
Jinsheng YANG
;
Xiangqun SHI
;
Junqiang YAN
- Publication Type:Journal Article
- Keywords:
ginsenoside Rd;
cerebral ischemia;
NR2B receptor;
endonuclease G
- From:
International Journal of Cerebrovascular Diseases
2008;16(8):571-575
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe the effect of ginsenoside Rd pretreatment on the expressions of N-methyl-D-aspartate(NMDA)receptor subunit NR2 B protein and endonuclease G(EndoG)in basal ganglia region after cerebral focal ischemia-reperfusion in rats and to investigate possible mechanism of ginsenoside Rd in the treatment of ischemic stroke.Methods:A rat model of middle cerebral artery occlusion(MCAO)was induced by intraluminal filament method.The expressions of NR2B and EndoG in basal ganglia region for focal cerebral iSChemia 1 hour,and 1,6,24 and 72 hours reperfusion were detected by immunohistochemical staining and image analysis method.The effects of ginsenoside Rd on the expressions of FaxioG and NR2B and the volume of cerebral infarction were evaluated.Results:The positive expression of NR2B in basal ganglia region on the ischemic side in ischemia-reperfusion group was increased significantly.The expression of EndoG in the nucleus was notable;the positive expressions of NR2B and EndoG at different reperfusion time points in ginsenoside Rd pretreatment group were decreased significantly(P<0.05 or P<0.01),and the volume of cerebral infarction was reduced significantly(P<0.01).Conclusions:The expressions of NMDA receptor subunit NR2B protein and apoptosis-inducing factor EndoG were increased significantly after cerebral focal ischemia reperfusion;ginsenoside Rd pretreatment may significantly reduce the expressions of NR2B and EndoG.It reduces the volume of cerebral infarction by inhibiting excitatory neurotoxicity and blocking neuronal apoptosis,and thus plays a role in neuroprotection.
