Neuroprotective effects of tanshinone II A on vascular dementia in rats.
- Author:
Zhi HE
1
;
Zhihong PAN
;
Wenhong LU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Dementia, Vascular; drug therapy; metabolism; physiopathology; Disease Models, Animal; Diterpenes, Abietane; Drugs, Chinese Herbal; administration & dosage; Humans; Male; Malondialdehyde; metabolism; Maze Learning; drug effects; Memory; drug effects; Neuroprotective Agents; administration & dosage; Phenanthrenes; administration & dosage; Random Allocation; Rats; Rats, Sprague-Dawley
- From: China Journal of Chinese Materia Medica 2010;35(14):1883-1886
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the underlying neuroprotective mechanisms of Tanshinone II A (TSA) on rat cerebral ischemia in vivo.
METHODStudy of TSA on rat cerebral ischemia in vivo: Male SD rats were divided into four groups (sham-operated, ischemic and treated group (lower dose and higher dose). Chronic cerebral ischemmia after permanent bilateral carotid artery ligation was introduced as an in vivo ischemic model. After ischemia impairment, TSA (2, 4 mg x kg(-1) x d(-1)) was administrated by ip for 30 days in treated group. We used Morris water maze to investigate the learning and memory. Levels of malondialdehyde (MDA), activity of superoxide dismetase (SOD) and glutathione peroxidase (GPX) in brain tissue were detected by spectrophotometer. High-performance liquid chromatography (HPLC) with fluorescence detection was applied to measure the contents of glutamate and gamma-aminobutyric acid (GABA) in cortex and hippocampus.
RESULTSTSA can improve learning and memory deficits in vascular dementia. An elevation of SOD and GPX activity and decrease of MDA level were shown in TSA treated group after brain ischemia. Decreased glutamate and gamma-aminobutyric acid induced by chronic brain ischemia were markedly inhibited by TSA pretreatment.
CONCLUSIONThe neuroprotective effect of TSA are partly due to its functions as follow: anti-free radical injury; regulating the content of glutamate and gamma-aminobutyric acid.
