Comparison of gene expression profiles between rats of Shen deficiency syndrome and Shen-yang deficiency syndrome differentiated according to therapeutic efficacy of drugs used.
- Author:
Zi-Yin SHEN
1
;
Jian-Hua HUANG
;
Wei-Hua CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Adrenal Glands; drug effects; metabolism; Animals; Diagnosis, Differential; Epimedium; chemistry; Flavonoids; therapeutic use; Gene Expression Profiling; Hypothalamus; drug effects; metabolism; Lymphocytes; drug effects; metabolism; Male; Medicine, Chinese Traditional; Oligonucleotide Array Sequence Analysis; methods; Pituitary Gland; drug effects; metabolism; Rats; Rats, Sprague-Dawley; Syndrome; Time Factors; Yang Deficiency; diagnosis; drug therapy; genetics
- From: Chinese Journal of Integrated Traditional and Western Medicine 2007;27(2):135-137
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore similarity and difference of connotation between Shen deficiency syndrome (SDS) and Shen-yang deficiency syndrome (SYDS) on the molecular level.
METHODSThe senescent SD rats and corticosterone-treated rats were adopted for models of SDS and SYDS respectively, their syndrome was differentiated according to the therapeutic efficacy of treatment with epimedium flavonoids (EF). The gene expression profiles of hypothalamas, pituitary, adrenal gland and lymphocytes (HPAT axis) were detected before and after EF treatment using gene chip provided by Affymetrix company.
RESULTSAs compared with the young rats, the ageing rats and corticosterone-treated rats showed a significant down-regulation in highly consistent pattern, of various neurotransmitters of HPAT axis firstly, followed with that of growth and sex hormone related genes. EF could reverse the above genes expression in both models, and for SYDS model rats, it could also significantly up-regulate the gene expressions of heat shock protein, cytochrome P450 and thyroid stimulating hormone (TSH).
CONCLUSIONBoth SDS and SYDS model rats show connotation of Shen deficiency, and the substantial base of Shen-yang deficiency syndrome resides in the process of oxidative phosphorylation of energy metabolism accelerated by thyroid hormone.
