Effect of compound recipe Gengniankang on senile sexual hormone and expression of estrogen receptor in bone of climacteric female rats.
- Author:
Su-hui WU
1
;
Jing-fen SUN
;
Shu-zhen GUO
Author Information
- Publication Type:Journal Article
- MeSH: Age Factors; Animals; Apoptosis; Bone Density; drug effects; Bone and Bones; drug effects; metabolism; Climacteric; Drugs, Chinese Herbal; pharmacology; Estradiol; blood; Female; Follicle Stimulating Hormone; blood; Hormone Replacement Therapy; Hormones; blood; Luteinizing Hormone; blood; Osteoporosis; metabolism; Ovary; drug effects; physiology; Rats; Receptors, Estrogen; biosynthesis
- From: Chinese journal of integrative medicine 2005;11(3):205-208
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo compare the therapeutic effect of Compound Recipe Gengniankang ( GNK) with that of hormone replacement treatment (HRT) on climacteric female rats with osteoporosis, and to investigate the roles of estrogen and estrogen receptors in the mechanism of osteoporosis.
METHODSClimacteric female rats with osteoporosis were chosen and divided into three groups (GNK group, HRT group and control group). Apoptosis of ovarian granulose cells was measured by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) assay. Serum level of estradiol (E(2)), follicle stimulating hormone (FSH), luteinizing hormone (LH) were determined by the method of radioimmunoassay (RIA). Reverse transcriptase polymerase chain reaction (RT-PCT) technology was used to evaluate the expression of estrogen receptor (ER) in bone. Bone mineral density (BMD) was measured by double energy X-ray absorption (DEXA).
RESULTSIn the climacteric rats, BMD, serum E(2), ER mRNA expression in bone decreased remarkably, and serum FSH, LH and apoptosis of ovarian granulose cells increased obviously. After treating with GNK, all the indexes were reversed except serum E(2). The increase of E(2) was not significant.
CONCLUSIONGNK is effective on climacteric osteoporosis female rats. Its role is performed not by increasing serum E(2) but by enhancing ER in the bone and inhibiting apoptosis of ovarian granulose cells. GNK can deter further exhaustion of ovarian function.