Protective effect of jasminoidin on cascade of damage of cerebral ischemia in rats.
- Author:
Xiao-lei ZHU
1
;
Na ZHANG
;
Peng-tao LI
;
Yu-feng JIANG
;
Ya XU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Brain; metabolism; Brain Ischemia; etiology; metabolism; Drugs, Chinese Herbal; isolation & purification; pharmacology; Gardenia; chemistry; Infarction, Middle Cerebral Artery; complications; metabolism; Interleukin-1; blood; Male; Neuroprotective Agents; pharmacology; Phosphopyruvate Hydratase; blood; Plants, Medicinal; chemistry; Random Allocation; Rats; Rats, Sprague-Dawley; Saponins; isolation & purification; pharmacology; Tumor Necrosis Factor-alpha; metabolism; von Willebrand Factor; metabolism
- From: China Journal of Chinese Materia Medica 2004;29(11):1065-1068
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the protective effect of jasminoidin on cascade of damage of cerebral ischemia.
METHODThe rats were randomly divided into four groups: sham-operated group, ischemic group, the jasminoidin-treatment group and PNS-treatment group. Focal cerebral ischemia was produced by permanent occlusion of left middle cerebral artery (PMCAO) in rats. Radioimmunoassay (RIA) was utilized to identify the content of tumor necrosis factor-alpha (TNF-alpha) and interlukin 1beta (IL-1beta) in brain tissue of rats following ischemia. and that of Neuron-specific enolase (NSE) in rat's serum was observed too. The plasma concentration of vonWillebrand factor (vWF) was identified by enzyme-linked immunoadsordent assay (ELISA).
RESULTAfter 12 h and 24 h of ischemia, the contents of TNF-alpha and IL-1beta and vWF as well as on NSE showed concomitant increase. Jasminoidin dramatically inhibited the increase of TNF-alpha and IL-1beta after 12 h and 24 h of ischemia, and repressed the increase of vWF after 12 h and 24 h of ischemia too. However, the influence of jasminodin NSE after 12 h and 24 h of ischemia was not significant.
CONCLUSIONJasminoidin had good effect on repressing the expression of TNF-alpha and IL-1beta as well as vWF caused by cerebral ischemia, thus it manifested the effect of relieving the damage to vascular endothelial cell and blocking the progress of cascade damage of cerebral ischemia through inhibiting the process of inflammation.
