https://scholars.lib.ntu.edu.tw/handle/123456789/204972
標題: | Nitric Oxide Induces Osteoblast Apoptosis through the De Novo Synthesis of Bax Protein | 作者: | CHEN, RUEI-MING LIU, HWA-CHANG WANG, JYH-HORNG |
關鍵字: | CELL-DEATH;BONE;SYNTHASE;ACTIVATION;6-NITROCHRYSENE;DIFFERENTIATION | 公開日期: | 2002 | 卷: | v.20 | 期: | n.2 | 起(迄)頁: | 295-302 | 來源出版物: | JOURNAL OF ORTHOPAEDIC RESEARCH | 摘要: | Nitric oxide (NO) plays a crucial role in the physiological and pathophysiological regulations of osteoblast functions. This Study is designed to evaluate the toxic effects of NO released by sodium nitroprusside (SNP), an NO donor, on neonatal Wistar rat calvarial osteoblasts from the analyses of cell viability, alkaline phosphatase (ALP ) activity, cell morphology, apoptotic cells, terminal deoxynucleotidyl transferase-mediated dUTP nick- end-label (TUNEL) assay, DNA ladder, and immunocytochemistry and Western blot for proapoptotic Bax protein. SNP increased the levels of nitrite, an oxidative product of NO. in the culture medium of osteoblasts in concentration- and time-dependent manners , and altered cell morphologies to round and shrinkage shapes . Administration of osteoblasts with SNP resulted in concentration- and time -dependent decreases of cell viability and ALP activity. Analysis of apoptotic cells revealed that SNP increased the percentages of osteoblasts processing apoptosis. Analyses of TUNEL and DNA ladder showed that SNP caused DNA fragmentation. Pretreatment with cycloheximide, an inhibitor of protein synthesis. partially blocked SNP-induced osteoblast apoptosis. Imunocytochemical and immunoblotting analyses revealed that SNP increased Bax protein in osteoblasts. This study suggests that SNP Could increase the levels of NO in osteoblasts, and cause osteoblast apoptosis possibly through the de novo synthesis of proapoptotic Bax protein. (C) 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. |
URI: | http://ntur.lib.ntu.edu.tw//handle/246246/99137 |
顯示於: | 醫學系 |
在 IR 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。