Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add filters








Year range
1.
Biomedical and Environmental Sciences ; (12): 83-89, 2003.
Article in English | WPRIM | ID: wpr-264291

ABSTRACT

<p><b>OBJECTIVE</b>To observe the effects of two main isoflavones, daidzein and genistein on the bone-nodule formation in rat calvaria osteoblasts in vitro.</p><p><b>METHODS</b>Osteoblasts obtained from newborn Sprague-dawley rat calvaria were cultured for several generations. The second generation cells were cultured in Minimum Essential Medium supplemented with ascorbic acid and Na-beta-glycerophosphate for several days, in the presence of daidzein and genistein, with or without the estrogen receptor antagonist ICI 182780. Number of nodules was counted at the end of the incubation period (day 20) by staining with Alizarin Red S calcium stain. The release of osteocalcin, as a marker of osteoblast activity, was also determined on day 7 and day 12 during the incubation period.</p><p><b>RESULTS</b>Compared with the control, the numbers of nodules were both increased by incubation with daidzein and genistein. 17 beta-estradiol was used as a positive control and proved to be a more effective inducer of the increase in bone-nodules formation that daidzein and genistein. The release of osteocalcin into culture media was also increased in the presence of daidzein and genistein, as well as 17 beta-estradiol on day 7 and day 12 (day 12 were higher). The estrogen receptor antagonist ICI 182780 completely blocked the genistein- and 17 beta-estradiol-induced increase of nodule numbers and osteocalcin release in osteoblasts. However, the effects induced by daidzein could not be inhibited by ICI 182780.</p><p><b>CONCLUSION</b>These findings suggest that geinistein can stimulate bone-nodule formation and increase the release of osteocalcin in rat osteoblasts. The effects, like those induced by 17 beta-estradiol, are mediated by the estrogen receptor dependent pathway. Daidzein also can stimulate bone-nodule formation and increase the release of osteocalcin in rat osteoblasts, but it is not, at least not merely, mediated by the estrogen receptor dependent pathway.</p>


Subject(s)
Animals , Rats , Cells, Cultured , Genistein , Pharmacology , Isoflavones , Pharmacology , Osteoblasts , Cell Biology , Metabolism , Osteocalcin , Osteogenesis , Rats, Sprague-Dawley , Skull , Cell Biology , Metabolism
2.
Acta Academiae Medicinae Sinicae ; (6): 275-279, 2003.
Article in Chinese | WPRIM | ID: wpr-350109

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the therapeutic effect of recombinant human parathyroid hormone(1-34) [rhPTH(1-34)] on osteoporosis of ovariectomized rats.</p><p><b>METHODS</b>The model of osteoporosis was formed after 3 months of ovariectomy with 6-month age of 80 rats. Another 20 rats was control of sham operation. rhPTH(1-34) was subcutaneously injected once daily with 5, 10, 20, 40 micrograms/kg for 3 months. There were 10 rats in each group. The control of therapy included Salmon Calcitonin to 10 rats and Alendronate sodium to 10 rats. The bone weight of dry and ash, bone mineral density, bone biomechanical property, trabecular area, bone mineral deposition and serum alkaline phosphatase, Ca, P and urinary Pyridinoline/creatin (Pyd/Cr) were measured after the end of therapy.</p><p><b>RESULTS</b>When administered to animals as a single subcutaneous injection once daily, rhPTH(1-34) increased obviously bone mass, bone biomechanical property and trabecular area, as well as bone deposition compared with the animals of control group. The bone architecture was ultimately improved by rhPTH(1-34) therapy.</p><p><b>CONCLUSIONS</b>Rats of ovariectomized-induced osteoporosis possess obvious effect of treatment with low dose of rhPTH(1-34) administered once daily.</p>


Subject(s)
Animals , Female , Rats , Osteoporosis , Drug Therapy , Ovariectomy , Recombinant Proteins , Therapeutic Uses , Teriparatide , Therapeutic Uses
SELECTION OF CITATIONS
SEARCH DETAIL