Effect of yizhi jiannao granule concentration fluid on the differential expression protein in entorhinal area tissue of senescence accelerated mouse P8.
- Author:
Ting ZHANG
1
;
Ke-Li DONG
;
Guang-Cheng LI
Author Information
- Publication Type:Journal Article
- MeSH: Aging; metabolism; Alzheimer Disease; metabolism; Animals; Disease Models, Animal; Drugs, Chinese Herbal; pharmacology; Entorhinal Cortex; metabolism; Male; Mice; Neurons; metabolism; Oxidative Stress; Proteins; metabolism; Proteome; analysis; Proteomics
- From: Chinese Journal of Integrated Traditional and Western Medicine 2010;30(5):504-508
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the mechanism of Yizhi Jiannao Granule (YZJN) in treating Alzheimer's disease (AD) on proteomic level by analyzing the differential expression proteins in entorhinal cortex tissue of senescence accelerated mouse P8 (SAMP8) treated with YZJN.
METHODSSix-month old SAMP8 were randomly divided into 3 groups, the model group, the YZJN group and the control group, 10 mice in each group. The model group was untreated with free water access, the YZJN group was treated with concentrated water extract of YZJN 0.3 g per day via gastric perfusion, and the control group was perfused with equal volume of double distilled water. The total protein in entorhinal cortex tissue of mice was extracted after an 8-week treatment with two-dimensional gel electrophoresis, and the differential expression protein spots were separated for identification through peptide mass fingerprint analysis and database searching.
RESULTSThirty-two protein spots expressed differentially between the YZJN group and the model group were found, and 14 differential expression proteins were identified, including NADH dehydrogenase iron-sulfur protein 6, Rho-GDP dissociation inhibitor alpha, beta2-globin, phosphoglyceric kinase, etc, their functions involved mitochondria energy metabolism, oxidative stress and neuron function.
CONCLUSIONYZJN could regulate multiple protein expressions in entorhinal cortex tissues of SAMP8, suggesting that it has multi-target therapeutic action and its mechanism in treating AD is possibly realized by way of improving mitochondria function, antagonizing oxidation stress, preventing nerve cell apoptosis and protecting neurons.