Role of dehydroepiandrosterone in management of glucocorticoid-induced secondary osteoporosis in female rats

被引:8
作者
Ahmed, Hanaa H. [1 ]
Morcos, Nadia Y. S. [2 ]
Eskander, Emad F. [1 ]
Seoudi, Dina M. S. [2 ]
Shalby, Aziza B. [1 ]
机构
[1] Natl Res Ctr, Dept Hormones, Cairo, Egypt
[2] Ain Shams Univ, Fac Sci, Dept Biochem, Cairo, Egypt
关键词
Prednisolone; Osteoporosis; DHEA; Bone biomarkers; Rats; POSTMENOPAUSAL WOMEN; BONE METABOLISM; LONG-TERM; THERAPY; DHEA; DEXAMETHASONE; OSTEOBLASTS; SUPPRESSION; INDUCTION; AROMATASE;
D O I
10.1016/j.etp.2011.01.004
中图分类号
R36 [病理学];
学科分类号
100103 [病原生物学];
摘要
The current study aimed to evaluate the potential role of dehydroepiandrosterone (DHEA) in the protection and intervention of glucocorticoid-induced secondary osteoporosis in female rats. For this purpose this study was conducted on five groups of female Sprague Dawley rats which were classified into: (1) negative control group received saline as vehicle, (2) osteoporotic group orally administered with prednisolone (5 mg/kg b.wt.) daily for six months, (3) positive control group orally administered with DHEA (250 mg/kg b.wt.) three times weekly for six months, (4) protective group orally administered with prednisolone daily with simultaneous oral administration of DHEA three times weekly for six months and (5) therapeutic group orally administered with prednisolone daily for six months then orally administered with DHEA three times weekly for other six months. The obtained data revealed that prednisolone administration resulted in significant decrease in serum osteocalcin (OC), 1,25-dihydroxyvitamin D-3 (1,25-(OH)(2) D-3) and osteoprotegerin (OPG) levels accompanied with significant increase in serum parathyroid hormone (PTH) and receptor activator nuclear factor kappa B ligand (RANKL) levels. Histopathological investigation of left femur bone showed that prednisolone administration produced compression of the reduced articular surface and atrophy of the epiphyseal bone. On the other hand, DHEA supplementation to osteoporotic rats increased serum OC, 1,25-(OH)(2) D-3 and OPG levels while decreased serum PTH and RANKL levels. Moreover, DHEA administration resulted in restoration of intact epiphyseal bony structure and articular surface. In conclusion, DHEA via its control on glucocorticoid activity and androgenic action provided potent effect on bone. (C) 2011 Elsevier GmbH. All rights reserved.
引用
收藏
页码:659 / 664
页数:6
相关论文
共 39 条
[1]
Chronic glucocorticoid treatment alters spontaneous pulsatile parathyroid hormone secretory dynamics in human subjects [J].
Bonadonna, S ;
Burattin, A ;
Nuzzo, M ;
Bugari, G ;
Rosei, EA ;
Valle, D ;
Iori, N ;
Bilezikian, JP ;
Veldhuis, JD ;
Giustina, A .
EUROPEAN JOURNAL OF ENDOCRINOLOGY, 2005, 152 (02) :199-205
[2]
BOUILLON R, 1990, CLIN CHEM, V36, P271
[3]
DHEA in bone and joint diseases [J].
Cormier, C ;
Souberbielle, JC ;
Kahan, A .
JOINT BONE SPINE, 2001, 68 (06) :588-594
[4]
Potential new drug targets for osteoporosis [J].
Deal, Chad .
NATURE CLINICAL PRACTICE RHEUMATOLOGY, 2009, 5 (01) :20-27
[5]
Glucocorticoid suppression of IGF I transcription in osteoblasts [J].
Delany, AM ;
Durant, D ;
Canalis, E .
MOLECULAR ENDOCRINOLOGY, 2001, 15 (10) :1781-1789
[6]
Osteoclastogenesis in Children with 21-Hydroxylase Deficiency on Long-Term Glucocorticoid Therapy: The Role of Receptor Activator of Nuclear Factor-κB Ligand/Osteoprotegerin Imbalance [J].
Faienza, Maria Felicia ;
Brunetti, Giacomina ;
Colucci, Silvia ;
Piacente, Laura ;
Ciccarelli, Maria ;
Giordani, Lucia ;
Del Vecchio, Giovanni Carlo ;
D'Amore, Massimo ;
Albanese, Livia ;
Cavallo, Luciano ;
Grano, Maria .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2009, 94 (07) :2269-2276
[7]
Cortisol and the renal handling of electrolytes: role in glucocorticoid-induced hypertension and bone disease [J].
Ferrari, P .
BEST PRACTICE & RESEARCH CLINICAL ENDOCRINOLOGY & METABOLISM, 2003, 17 (04) :575-589
[8]
Effects of oral dehydroepiandrosterone on bone density in young women with anorexia nervosa: A randomized trial [J].
Gordon, CM ;
Grace, E ;
Emans, SJ ;
Feldman, HA ;
Goodman, E ;
Becker, KA ;
Rosen, CJ ;
Gundberg, CM ;
LeBoff, MS .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2002, 87 (11) :4935-4941
[9]
MONOCYTE 1-ALPHA-HYDROXYLASE REGULATION - INDUCTION BY INFLAMMATORY CYTOKINES AND SUPPRESSION BY DEXAMETHASONE AND UREMIA TOXIN [J].
GYETKO, MR ;
HSU, CH ;
WILKINSON, CC ;
PATEL, S ;
YOUNG, E .
JOURNAL OF LEUKOCYTE BIOLOGY, 1993, 54 (01) :17-22
[10]
The effects of dexamethasone and dehydroepiandrosterone (DHEA) on cytokines and receptor expression in a human osteoblastic cell line: Potential steroid-sparing role for DHEA [J].
Harding, G. ;
Mak, Y. T. ;
Evans, B. ;
Cheung, J. ;
MacDonald, D. ;
Hampson, G. .
CYTOKINE, 2006, 36 (1-2) :57-68