Potential role of leptin against glucocorticoid-induced secondary osteoporosis in adult female rats.

نویسندگان

  • H H Ahmed
  • N Y S Morcos
  • E F Eskander
  • D M S Seoudi
  • A B Shalby
چکیده

OBJECTIVES The present study assessed the potential role of leptin administration in the protection and intervention against glucocorticoid-induced secondary osteoporosis in female rats. MATERIALS AND METHODS For this purpose five groups of female Sprague Dawley rats were classified into: (1) negative control group in which the healthy rats received saline as vehicle, (2) a group orally administered with prednisolone (5 mg kg b.wt.-1) daily for six months (osteoporotic group), (3) a group subcutaneously administered with leptin (400 microg kg b.wt.-1) three times weekly for six months (positive control), (4) a group orally administered with prednisolone daily with simultaneous subcutaneous administration of leptin three times weekly for six months (protective group), and (5) a group orally administered with prednisolone daily for six months then subcutaneously administered with leptin three times weekly for other six months (therapeutic group). RESULTS The obtained data revealed that prednisolone administration resulted in significant decrease in serum osteoprotegerin (OPG) level accompanied with significant increase in serum receptor activator of nuclear factor-κB ligand (RANKL) and beta2-microglobulin levels in comparison with the negative control group. Moreover, prednisolone significantly decreased bone mineral density and content of different areas of the right femur bones as compared to the negative control group. Furthermore, administration of leptin with/after stopping prednisolone administration resulted in a marked modulation in the majority of bone biomarkers as well as improvement in bone mineral density and content. CONCLUSIONS Leptin provided promising effect on bone through its direct action on bone and matrix mineralization.

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عنوان ژورنال:
  • European review for medical and pharmacological sciences

دوره 16 10  شماره 

صفحات  -

تاریخ انتشار 2012