中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2013年
50期
8621-8628
,共8页
王翔%郭海玲%赵咏芳%詹红生%石印玉
王翔%郭海玲%趙詠芳%詹紅生%石印玉
왕상%곽해령%조영방%첨홍생%석인옥
组织构建%骨组织构建%骨质疏松%骨质量%骨强度%Ⅰ型胶原%交联%双膦酸盐%骨基质%骨结构%国家自然科学基金
組織構建%骨組織構建%骨質疏鬆%骨質量%骨彊度%Ⅰ型膠原%交聯%雙膦痠鹽%骨基質%骨結構%國傢自然科學基金
조직구건%골조직구건%골질소송%골질량%골강도%Ⅰ형효원%교련%쌍련산염%골기질%골결구%국가자연과학기금
背景:双膦酸盐可以提高骨密度、抑制骨吸收的作用已被临床所证实,但其对于骨骼基质结构的影响研究较少。<br> 目的:实验通过观察双膦酸盐类药物--阿仑膦酸钠对骨结构及骨基质代谢的影响,探讨阿仑膦酸钠改善骨质量、提高骨强度的骨基质调控机制。<br> 方法:实验建立去卵巢大鼠模型,用阿仑膦酸钠进行干预,同时设置模型组和假手术组进行对照。运用骨骼影像学、骨组织病理学和骨生物力学检测技术与酶联免疫吸附法观察阿仑膦酸钠对骨丢失大鼠骨密度、骨代谢、骨生物力学性能和骨结构的影响。<br> 结果与结论:药物干预后4,8,12周,阿仑膦酸钠组骨密度均高于模型组(P<0.05);药物干预8周后,与模型组相比,阿仑膦酸钠组骨代谢指标尿脱氧吡啶诺啉,血清Ⅰ型胶原羧基端前肽水平均降低(P<0.05),腰椎和股骨的最大载荷、最大压强、模量以及Ⅰ型胶原不同交联形式的尿吡啶啉/脱氧吡啶啉值均增高(P<0.05)。结果证实,阿仑膦酸钠能够对抗因雌激素缺乏导致大鼠骨量的丢失,提高生物力学性能,改善骨基质结构,同时恢复因去卵巢所导致的Ⅰ型胶原交联组分的改变。
揹景:雙膦痠鹽可以提高骨密度、抑製骨吸收的作用已被臨床所證實,但其對于骨骼基質結構的影響研究較少。<br> 目的:實驗通過觀察雙膦痠鹽類藥物--阿崙膦痠鈉對骨結構及骨基質代謝的影響,探討阿崙膦痠鈉改善骨質量、提高骨彊度的骨基質調控機製。<br> 方法:實驗建立去卵巢大鼠模型,用阿崙膦痠鈉進行榦預,同時設置模型組和假手術組進行對照。運用骨骼影像學、骨組織病理學和骨生物力學檢測技術與酶聯免疫吸附法觀察阿崙膦痠鈉對骨丟失大鼠骨密度、骨代謝、骨生物力學性能和骨結構的影響。<br> 結果與結論:藥物榦預後4,8,12週,阿崙膦痠鈉組骨密度均高于模型組(P<0.05);藥物榦預8週後,與模型組相比,阿崙膦痠鈉組骨代謝指標尿脫氧吡啶諾啉,血清Ⅰ型膠原羧基耑前肽水平均降低(P<0.05),腰椎和股骨的最大載荷、最大壓彊、模量以及Ⅰ型膠原不同交聯形式的尿吡啶啉/脫氧吡啶啉值均增高(P<0.05)。結果證實,阿崙膦痠鈉能夠對抗因雌激素缺乏導緻大鼠骨量的丟失,提高生物力學性能,改善骨基質結構,同時恢複因去卵巢所導緻的Ⅰ型膠原交聯組分的改變。
배경:쌍련산염가이제고골밀도、억제골흡수적작용이피림상소증실,단기대우골격기질결구적영향연구교소。<br> 목적:실험통과관찰쌍련산염류약물--아륜련산납대골결구급골기질대사적영향,탐토아륜련산납개선골질량、제고골강도적골기질조공궤제。<br> 방법:실험건립거란소대서모형,용아륜련산납진행간예,동시설치모형조화가수술조진행대조。운용골격영상학、골조직병이학화골생물역학검측기술여매련면역흡부법관찰아륜련산납대골주실대서골밀도、골대사、골생물역학성능화골결구적영향。<br> 결과여결론:약물간예후4,8,12주,아륜련산납조골밀도균고우모형조(P<0.05);약물간예8주후,여모형조상비,아륜련산납조골대사지표뇨탈양필정낙람,혈청Ⅰ형효원최기단전태수평균강저(P<0.05),요추화고골적최대재하、최대압강、모량이급Ⅰ형효원불동교련형식적뇨필정람/탈양필정람치균증고(P<0.05)。결과증실,아륜련산납능구대항인자격소결핍도치대서골량적주실,제고생물역학성능,개선골기질결구,동시회복인거란소소도치적Ⅰ형효원교련조분적개변。
BACKGROUND:Bisphosphonates that can increase bone density and inhibit bone resorption have been clinical y confirmed, but the structure of the bone matrix has been less studied. <br> OBJECTIVE:To observe the effects of alendronate on bone structure and bone matrix metabolism, and then to investigate the control ing mechanism by which alendronate improves bone mass and increase bone intensity. <br> METHODS:An ovariectomized rat model was prepared and intervened with alendronate as treatment group. Model and sham-surgery groups were set as controls. Alendronate effects on bone mineral density, bone metabolism, bone biomechanics, and bone structure were observed in bone loss rats using bone imaging, bone tissue pathology and biomechanical test and enzyme-linked immunosorbent assay. <br> RESULTS AND CONCLUSION:Alendronate intervention could fight against bone loss as compared with model group at weeks 4, 8, and 12 after treatment (P<0.05). Compared with the model group, the expression of urinary deoxypyridinoline and serum carboxyterminal propeptide of type Ⅰ procol agen was decreased significantly after alendronate intervention (P<0.05);the maximal load, maximal pressure and modelus on the lumbar vertebrae and femur were increased as wel as ratio of urinary pyridinoline/deoxypyridinoline of type Ⅰ procol agen (P<0.05). These findings suggest that alendronate intervention can inhibit bone loss in rats induced by estrogen deficiency, increase biomechanical properties, improve bone matrix structure, and meanwhile, recover the Ⅰ col agen crosslinking component due to ovariectomy.