Effects of ginsenoside Rg1 on endothelial cell adhesion after cerebral ischemia-reperfusion in rats
- VernacularTitle:人参皂苷Rg1对大鼠脑缺血再灌注损伤及内皮细胞粘附作用的影响
- Author:
Xiamin HU
;
Changkai YAN
;
Shiqiang XU
;
Xianmin HU
;
Fandian ZENG
- Publication Type:Journal Article
- Keywords:
ginsenoside Rg1;
cerebral ischemia;
intercellular adhesion molecule-1;
E-selectin;
peroxidase
- From:
Chinese Journal of Pharmacology and Toxicology
2006;20(1):19-25
- CountryChina
- Language:Chinese
-
Abstract:
AIM To investigate if inhibiting neutrophil infiltration and adhesion molecules expression is a part of the mechanisms of ginsenoside Rg1 protecting from cerebral injury after cerebral ischemia-reperfusion. METHODS Rats were pretreated with ginsenoside Rg1 25, 50 and 100 mg·kg-1·d-1, ig, for 7 d, respectively, then subjected to cerebral ischemia (middle cerebral artery occlusion) for 2 h and reperfusion for 22 h. The infarct volume and the neurological deficit were determined by TTC staining and Longa's scoring, respectively. The infiltration of neutrophils was evaluated by measuring the activity of myeloperoxidase (MPO). The expressions of intercellular adhesion molecule-1 (ICAM-1) and E-selectin were analyzed by Western blot. The permeability of the blood-brain barrier was evaluated by measurement of Evans blue content in brain tissue with spectrophotometer at 4 h after reperfusion. RESULTSCompared with vehicle-treated group, ginsenoside Rg1 (50 and 100 mg·kg-1·d-1) treatment significantly reduced infarct volume and elevated permeability of blood-brain barrier, alleviated the neurological deficit, and inhibited protein expressions of ICAM-1 and E-selectin in brain tissue. CONCLUSION Ginsenoside Rg1 has protective effects on cerebral injury induced by ischemia-reperfusion through inhibiting neutrophil infiltration and expression of the adhesion molecules.
