中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2015年
40期
6402-6407
,共6页
曹鲁宁%崔敏%于灵芝%张娜%赵旭
曹魯寧%崔敏%于靈芝%張娜%趙旭
조로저%최민%우령지%장나%조욱
实验动物%骨及关节损伤动物模型%唑来膦酸%糖尿病%骨质疏松%成骨细胞%骨形态发生蛋白2%Noggin%骨密度%骨碱性磷酸酶
實驗動物%骨及關節損傷動物模型%唑來膦痠%糖尿病%骨質疏鬆%成骨細胞%骨形態髮生蛋白2%Noggin%骨密度%骨堿性燐痠酶
실험동물%골급관절손상동물모형%서래련산%당뇨병%골질소송%성골세포%골형태발생단백2%Noggin%골밀도%골감성린산매
背景:糖尿病引起的骨质疏松作为常见的继发性骨质疏松,近年来越来越受到重视;唑来膦酸作为新型治疗骨质疏松的药物,其对体内成骨细胞的作用尚未完全清楚。目的:观察1型糖尿病大鼠股骨干骺端骨形态发生蛋白2与Noggin的表达变化,以及唑来膦酸的干预作用。方法:随机取130只Wistar大鼠腹腔注射链脲佐菌素建立1型糖尿病模型,3 d后连续3次血糖>16.7 mmol/L鼠为造模成功鼠,共120只,随机等分为模型组、预防组和治疗组。后2组大鼠分别在造模后当天和2周后一次性静脉给予唑来膦酸(0.1 mg/kg)。另取40只大鼠注射柠檬酸缓冲液作为对照组。结果与结论:与对照组相比,模型组大鼠股骨骨密度、血清碱性磷酸酶水平、股骨骨形态发生蛋白2 mRNA表达水平明显降低(P <0.05),Noggin mRNA表达水平显著升高(P <0.05)。与模型组相比,预防组和治疗组大鼠骨密度和骨形态发生蛋白2 mRNA表达水平显著升高(P <0.05),Noggin mRNA表达水平显著降低(P <0.05),血清骨碱性磷酸酶水平也逐渐恢复。提示1型糖尿病大鼠骨代谢紊乱在病程早期即出现,而应用唑来膦酸可以促进骨形成,增加骨密度,改善骨代谢。
揹景:糖尿病引起的骨質疏鬆作為常見的繼髮性骨質疏鬆,近年來越來越受到重視;唑來膦痠作為新型治療骨質疏鬆的藥物,其對體內成骨細胞的作用尚未完全清楚。目的:觀察1型糖尿病大鼠股骨榦骺耑骨形態髮生蛋白2與Noggin的錶達變化,以及唑來膦痠的榦預作用。方法:隨機取130隻Wistar大鼠腹腔註射鏈脲佐菌素建立1型糖尿病模型,3 d後連續3次血糖>16.7 mmol/L鼠為造模成功鼠,共120隻,隨機等分為模型組、預防組和治療組。後2組大鼠分彆在造模後噹天和2週後一次性靜脈給予唑來膦痠(0.1 mg/kg)。另取40隻大鼠註射檸檬痠緩遲液作為對照組。結果與結論:與對照組相比,模型組大鼠股骨骨密度、血清堿性燐痠酶水平、股骨骨形態髮生蛋白2 mRNA錶達水平明顯降低(P <0.05),Noggin mRNA錶達水平顯著升高(P <0.05)。與模型組相比,預防組和治療組大鼠骨密度和骨形態髮生蛋白2 mRNA錶達水平顯著升高(P <0.05),Noggin mRNA錶達水平顯著降低(P <0.05),血清骨堿性燐痠酶水平也逐漸恢複。提示1型糖尿病大鼠骨代謝紊亂在病程早期即齣現,而應用唑來膦痠可以促進骨形成,增加骨密度,改善骨代謝。
배경:당뇨병인기적골질소송작위상견적계발성골질소송,근년래월래월수도중시;서래련산작위신형치료골질소송적약물,기대체내성골세포적작용상미완전청초。목적:관찰1형당뇨병대서고골간후단골형태발생단백2여Noggin적표체변화,이급서래련산적간예작용。방법:수궤취130지Wistar대서복강주사련뇨좌균소건립1형당뇨병모형,3 d후련속3차혈당>16.7 mmol/L서위조모성공서,공120지,수궤등분위모형조、예방조화치료조。후2조대서분별재조모후당천화2주후일차성정맥급여서래련산(0.1 mg/kg)。령취40지대서주사저몽산완충액작위대조조。결과여결론:여대조조상비,모형조대서고골골밀도、혈청감성린산매수평、고골골형태발생단백2 mRNA표체수평명현강저(P <0.05),Noggin mRNA표체수평현저승고(P <0.05)。여모형조상비,예방조화치료조대서골밀도화골형태발생단백2 mRNA표체수평현저승고(P <0.05),Noggin mRNA표체수평현저강저(P <0.05),혈청골감성린산매수평야축점회복。제시1형당뇨병대서골대사문란재병정조기즉출현,이응용서래련산가이촉진골형성,증가골밀도,개선골대사。
BACKGROUND:Osteoporosis caused by diabetes melitus as common secondary osteoporosis has been paid more and more attention recently. Zoledronic acid serves as a novel drug for osteoporosis, and its effect on osteoblasts in vivo remains unclear. OBJECTIVE:To investigate the changes of the expression of bone morphogenetic protein 2 andNoggin in the femur of type 1 diabetes melitus rats and the effect of zoledronic acid on them. METHODS:Models of type 1 diabetes melitus were established by intraperitoneal injection of streptozotocin in 130 Wistar rats. 3 days later, rats with blood sugar > 16.7 mmol/L for three consecutive times were considered as successful models, 120 in total. These models were randomly divided into model, prevention and treatment groups. Rats in the prevention and treatment groups were intravenously administered zoledronic acid (0.1 mg/kg) on the day of modeling and 2 weeks after model establishment. An additional 40 rats were injected with citrate buffer solution as control group. RESULTS AND CONCLUSION: Compared with the control group, femur bone mineral density, serum alkaline phosphatase levels, and femur bone morphogenetic protein 2 mRNA expression levels were significantly lower in the model group (P < 0.05), butNoggin mRNA expression significantly increased (P < 0.05). Compared with the model group, bone mineral density and bone morphogenetic protein 2 mRNA expression levels were significantly higher in the prevention and treatment groups (P < 0.05), butNoggin mRNA expression significantly lower (P < 0.05), and serum alkaline phosphatase levels gradualy restored. These results indicated that the bone metabolic disturbance occurs in early stage in rats with type 1 diabetes melitus. Zoledronic acid can promote bone formation, increase bone density, and improve bone metabolism.