Protective effect of Naoyikang on the Alzheimer's disease model mice induced by D-galactose and NaNO2.
- Author:
Yan ZHU
1
;
Ai-Ling ZHOU
;
Jia-Hui MAO
;
Ya-E HU
;
Hai-Yan SHI
Author Information
- Publication Type:Journal Article
- MeSH: Alzheimer Disease; chemically induced; drug therapy; Animals; Disease Models, Animal; Drugs, Chinese Herbal; therapeutic use; Female; Galactose; Male; Maze Learning; Mice; Mice, Inbred ICR; Neuroprotective Agents; therapeutic use; Phytotherapy; RNA, Messenger; genetics; metabolism; Random Allocation; Sodium Nitrite; Sodium-Potassium-Exchanging ATPase; metabolism; bcl-2-Associated X Protein; genetics; metabolism
- From: Chinese Journal of Applied Physiology 2008;24(3):296-300
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate the mechanisms of Naoyikang (Traditional Chinese Medicine) on the Alzheimer's Disease (AD) model mice induced by D-galactose (D-gal) and NaNO2.
METHODSThe mouse model was established by intraperitoneal injection of D-gal and NaNO2. The capacity of learning and memory was tested on mice with electrical maze; the content of nitric oxide (NO) and the activity of monoamine oxidase-B (MAO-B), glutathione peroxidase (GSH-PX), Na(+) -K(+) -ATP enzyme and Ca(2+) -ATP enzyme in cerebral cortex and hippocampus were assayed by biochemical methods; expression of Bax and Bcl-2 mRNA was detested by RT-PCR.
RESULTSNaoyikang could ameliorate the capacity of learning and memory of AD model mice and reduce MAO-B activity in the brain tissue and activate the activity of Na(+) -K(+) -ATP enzyme and Ca(2+) -ATP enzyme in the brain tissue and decrease the expression of Bax mRNA, but increase the expression of Bcl-2 mRNA in the model brain tissue.
CONCLUSIONNaoyikang could protect AD model mice induced by D-gal and NaNO2. It could modify the metabolism of monoamine neurotransmitter in brain through reducing MAO-B activity and protect neurons by activating the activity of Na(+) -K(+) -ATP enzyme and Ca(2+) -ATP enzyme and decrease Bax expression and increase Bcl-2 expression in the model brain tissue.
