[Syndrome differentiation through drug effects in mapping the two regulatory pathways of gene networks in Shen deficiency syndrome].

ABSTRACT

OBJECTIVE: To study the regulatory pathways and rules of the gene networks in Shen deficiency syndrome. METHODS: Tissues of hypothalamus, pituitary, adrenal, lymphocyte, bone, liver and kidney were taken as samples from 4 months' and 24 months' old SD rats and rats after treatment with Epimedium flavonoids (EF), differences of gene expression profile in Shen deficiency syndrome were studied repeatedly with gene chip rat expression set U230 2.0 array from Affymetrix Co. RESULTS: Gene expressions in the aged rats all decreased including neurotransmitter of gamma-aminobutyric acid (gammaGABA), gonadotropin releasing hormone (GnRH), thyrotropin-releasing hormone (TRH), thyroid stimulating hormone (TSH), growth hormone-releasing hormone receptor (GHRH), insulin-like growth factor (IGF) and binding proteins (IGFBP) in hypothalamus, pituitary and adrenal (HPA axis), cell growth-related gene, growth factor related protein, and immune regulatory genes such as interferon gamma (IFN-gamma), interleukin 4 (IL-4) and interleukin 6 (IL-6) in lymphocytes, parathyroid hormone (PTH), calcitonin, procollagen, collagen, connective tissue growth factor in bone, and oxidative phosphorylation genes such as cytochrome P450 and NADH dehydrogenase, glutamate dehydrogenase related with protein metabolism, and glucose-6-phosphatase related with glucose metabolism in liver, most of which were up-regulated after treatment with EF as well as genes related with ageing and cell cycle, such as cyclin B, metabolism related genes and proteins of sodium and chloride channel in kidney. CONCLUSION: Dysfunction of the two regulatory pathways of gene networks as nerve-endocrine-immunity and nerve-endocrine-bone metabolism exists in Shen deficiency syndrome differentiated by effects of drugs, which could be improved by strengthening Shen therapy.