• 대한수의학회지
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• 제39권5호
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• pp.974-985
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• 1999

Osteoporosis is defined as a decrease in bone mass that leads to an increased risk of fracture. The therapeutic effect of $1{\alpha}$,25 dihydroxycholecalciferol, the hormonal form of vitamin $D_3$ that mediates calcium translation in intestine and bone, on the healing process of fracture has still been controversial. These studies were designed to understand the healing process of normal fibular fracture, the osteoporotic changes after ovariectomy, and the therapeutic effects of $1{\alpha}$,25 dihydroxycholecalciferol on the osteoporotic fracture in rats. The simple transverse fractures of rat fibulae were produced with a rotating diamond saw. The changes of the biochemical and mechanical indices of rats were investigated. The mechanical study based on bending test revealed the healing of the fibular fracture in the 5th week after simple transverse fracture. The osteoporosis impaired more the healing of osteoporotic fibular fracture than normal non-osteoporotic fibular fracture. The healing process of osteoporotic fracture was facilitated by the treatment with $1{\alpha}$,25 dihydroxycholecalciferol, however, was delayed more than the healing process of normal fracture. The bone strength based on the bending test also confirmed this tendency. The bone strengths in the 5th week after fracture of normal bone, osteoporotic bone, and $1{\alpha}$,25 dihydroxycholecalciferol-treated osteoporotic bone were 75%, 41%, and 67%, respectively, in comparison with those of intact bone. In conclusion, $1{\alpha}$,25 dihydroxycholecalciferol was effective in promoting the osteoporotic fracture healing.

• Applied Microscopy
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• 제29권3호
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• pp.315-321
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• 1999

12주령 랫트의 정상 비골골절의 치유과정을 이해하고, 난소적출 후 비골골절의 치유과정과 난소적출 후 비골골절의 치유에 미치는 $1\alpha$, 25 dihyoxycholecalciferol의 영향을 알아보고자 실험을 실시한 결과 다음과 같은 결론을 얻었다. 비골의 골절은 골절유발 후 5주에 성숙된 신생골 조직으로 충만되어 조직형태학적으로 완전한 치유가 이루어졌다. 난소적출 후 골절의 치유는 정상골절의 치유보다 지연되었으나, $1\alpha$, 25 dihydroxycholecalciferol 투여 결과 골절유발 후 5주에 성숙된 신생골 조직으로 골절단이 충만되어 정상상태의 골절과 비슷하게 치유가 되었다. 이상의 결과를 종합해보면 랫트의 난소를 적출하여 여성호르몬의 결핍을 유발하면 난소적출 후 7주에는 골다공증이 발생되고, 골다공증은 정상상태의 골절에 비하여 약 1주일 이상 골절의 치유를 지연시켰으며, $1\alpha$, 25 dihydroxycholecalciferol을 투여하였을 경우 정상상태의 골절치유와 비슷한 경과를 나타내어 $1\alpha$, 25 dihydroxycholecalciferol은 골다공증성 골절의 치료에 있어서 효과있는 치료제라는 결론을 내릴 수 있었다.

• 한국전자현미경학회:학술대회논문집
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• 한국현미경학회 1999년도 제30차 추계학술대회
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• pp.24-24
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• 1999

• 한국식품영양과학회지
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• 제24권1호
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• pp.1-9
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• 1995

1, 25(OH)2-23ene-D3 is a novel vitamine D3 analog which has a double bond between C-23 and C-24. We describe the effects of this analog on cell differentiation and cell proliferation in vitro using the human histiocytic lymphoma cell line U937, and on calcium metabolism in rats in vivo. In the present investigation 1, 25(OH)2-23ene-D3 was compared to the natural metabolite of vitamin D3, 1$\alpha$, 25-dihydroxycholecalciferol[1, 25(OH)2-23ene-D3 was more potent than 1, 25(OH)2-23ene-D3 for inhibition of proliferation and induction of differentiation of U937 cells. Especially, its effect on induction of differentiation, as measured by superoxide production and nonspecific esterase(NSE) activity, was about 20-fold more potent that 1, 25(OH)2-23ene-D3. This analog morphologically and functionally differentiated U937 cells to monocyte-macrophage phenotype showing a decrease of N/C ratio in Giemsa staining and the increase of adherence ability to surface. Intraperitoneal administration of 1, 25(OH)2-23ene-D3 to rats showed that the compound had at least 50 times less activity than 1, 25(OH)2-23ene-D3 in causing hypercalcemia and hypercalciuria. The strong direct effects of 1, 25(OH)2-23ene-D3 on cell proliferation and cell differentiation, coupled with its decreased activity of calcium metabolism make this compound an interesting candidate for clinical studies including patients with leukemia, as well as several skin disorders, such as psoriasis.

• Imaging Science in Dentistry
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• 제35권3호
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• pp.127-131
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• 2005

Purpose : We performed the present study to investigate whether osteotropic hormomes play roles on the nitric oxide (NO) production in culture of ROS 17/12.8 osteoblastic cells. Materials and Methods : The osteoblastic cell line ROS17/2.8 cells were cultured In F12 medium supplemented with $5\%$ fetal bovine serum (FBS) at $37^{\circ}C$ in a humidified atmosphere of $5\%\;CO_2$ in air. ROS17/2.8 cells were plated in 96-well plates at a density of $2-3\times10^3cells/well$ and grown to confluence. Then the cells were pretreated with osteotropic hormones (parathyroid hormone (PTH) 20-500 ng/mL, 1, 25-dihydroxycholecalciferol $(1,\;25[OH]_2D_3)$ 1-100 nM; prostaglandin $E_2 (PGE_2)$ 20-500 ng/mL in the medium supplemented with $0.4\%$ FBS for 72 hours and the cells were treated with cytokines $(TNF{\alpha}\;and\;IFN{\gamma})$ in phenol red-free F12 medium for an additional 48 hours. NO synthesis was assessed by measuring the nitrite anion concentration, the reaction product of NO, in the cell culture medium using Griess reagent. Results : PTH and $1,\;25[OH]_2D_3$ pretreatment induced a significant increase in NO production in the presence of $TNF{\alpha}\;and\;IFN{\gamma}.\;PGE_2$ slightly induced NO production compared to the control group. But, $PGE_2$ pretreatment did not affect in NO production in the presence of $TNF{\alpha}\;and\;IFN{\gamma}$. Conclusions : These results suggest that the actions of osteotropic hormones In bone metabolism may be partially mediated by NO in the presence of cytokines.