Effects of icariin on beta-amyloid and neurotrophic factors in brain of mitochondrial deficiency model rats.
- Author:
Ru-Yi ZHANG
1
;
Li ZHANG
;
Hou-Xi AI
;
Lan ZHANG
;
Lin LI
Author Information
1. Department of Pharmacology, Xuanwu Hospital of Capital Medical University, Key Laboratory for Neurodegenerative Diseases of Ministry of Education, Beijing 100053, China. ruyiz2@sina.com
- Publication Type:Journal Article
- MeSH:
Amyloid;
metabolism;
Animals;
Brain;
drug effects;
metabolism;
Brain-Derived Neurotrophic Factor;
metabolism;
Disease Models, Animal;
Enzyme-Linked Immunosorbent Assay;
Flavonoids;
pharmacology;
therapeutic use;
Mitochondria;
drug effects;
metabolism;
pathology;
Mitochondrial Diseases;
drug therapy;
metabolism;
Nerve Growth Factor;
metabolism;
Nerve Growth Factors;
metabolism;
Rats;
Rats, Sprague-Dawley;
Receptor, trkB;
metabolism
- From:
China Journal of Chinese Materia Medica
2013;38(9):1285-1289
- CountryChina
- Language:Chinese
-
Abstract:
The purpose of the present study was to investigate the effects of icariin (ICA) on the content of beta-amyloid (Abeta) and the expression of neurotrophic factors in the brain of mitochondrial deficiency model rats. SD rats were infused subcutaneously with sodium azide, which is an inhibitor of mitochondrial respiratory chain complex IV, via a minipump (0. 5 mg . kg-1 h-1) for 28 days to establish the mitochondrial deficiency animal model. The activity of mitochondrial respiratory chain complex IV (i. e. cytochrome C oxidase, COX) in hippocampus was measured by biochemical methods. ELISA method was used to detect the content of Abeta in the brain. The expression of neurotrophic factors was detected by Western blot and immunohistochemistry methods. Image analysis was performed by Image-pro software. The results showed that chronic infusion of sodium azide by minipump induced a significant decrease in the activity of mitochondrial cytochrome C oxidase, an obvious increase in the content of Abeta, and a marked decline in the expression of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and its receptor TrkB in the brain of rats. Intragastrical administration of ICA (12 or 36 mg . kg-l) significantly ameliorated all these abnormalities in the model rats. In conclusion, ICA can increase mitochondrial activity, inhibit Abeta production, and enhance the expression of neurotrophic factors in the brain of model rats induced by sodium azide. The results suggested that ICA may have beneficial prospect for the treatment of Alzheimer's disease.
