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Effect of Sodium Nitroprusside on the Activation of Mouse Osteoblastic Cells

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dc.contributor.authorShin, Myung-Mi-
dc.contributor.authorKim, Gwan-Shik-
dc.date.accessioned2010-08-02T01:29:26Z-
dc.date.available2010-08-02T01:29:26Z-
dc.date.issued1996-
dc.identifier.citationInt. J. of Oral Biol. 20(1):25-30en
dc.identifier.issn1226-7155-
dc.identifier.urihttps://hdl.handle.net/10371/68840-
dc.description.abstractNitric oxide (NO), which is produced from arginine by a nitric oxide synthase, is a short-lived free radical that plays crucial role in a variety of tissues. Recently, it has been reported that NO is produced by osteoblast stimulated by lipopolysaccharide and several cytokines. Although NO appears to inhibit osteoclastic differentiation and activation, little is known about its possible role in osteoblastic function. Therefore, the effect of sodium nitroprusside (SNP), as a donor of nitric oxide, on osteoblastic activation in terms of alkaline phosphatase (ALP) activity and calcified nodule formation in the osteoblastic cells were studied. SNP increased not only the ALP activity but also the calcified nodule formation. ALP activity was enhanced significantly by the addition of SNP (30-300 μM)with 14-31% magnitude when compared with control. SNP also stimulated calcium phosphate - containing calcified matrix formation. The number of calcified nodules was increased significantly by continuous treatment of cultures with 30 μM SNP for 21 days. In addition to the recently reported inihbition of osteoclast function by NO, these results raise the possibility that NO could promote osteoblastic bone formation by stimulating osteoblastic function and mineralization as well.en
dc.language.isoenen
dc.publisherKorean Academy of Oral Biologyen
dc.subjectOsteoblasten
dc.subjectNitric oxideen
dc.subjectSodium nitroprussideen
dc.subjectAlkaline phosphataseen
dc.subjectCalcified noduleen
dc.subjectBone formationen
dc.titleEffect of Sodium Nitroprusside on the Activation of Mouse Osteoblastic Cellsen
dc.typeArticleen
dc.contributor.AlternativeAuthor신명미-
dc.contributor.AlternativeAuthor김관식-
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