维生素D缺乏对链霉素诱导的糖尿病小鼠骨缺损段ColⅡ、骨钙素、PPAR-γ和AP-2表达的影响  

Effect of vitamin D deficiency on the expression of ColⅡ,Osteocalcin,PPAR-γand AP-2 in bone defects of diabetic mice induced by streptomycin

作　　者：何婕 贺亚峰 何维 HE Jie;HE Ya-feng;HE Wei(Department of Outpatient Pharmacy,3201 Hospital Affiliated to Xi'an Jiaotong University,Hanzhong Shaanxi 723000,China;Department of Outpatient,Shaanxi Armed Police Corps Hospital,Xi'an Shaanxi 710086,China;Department of Urology,People's Hospital of Hanzhong City,Hanzhong Shaanxi 723000,China)

机构地区：[1]西安交通大学附属三二〇一医院门诊药房,陕西汉中723000 [2]武警陕西总队医院门诊部,陕西西安710086 [3]汉中市人民医院泌尿外科,陕西汉中723000

出　　处：《临床和实验医学杂志》2021年第14期1460-1463,共4页Journal of Clinical and Experimental Medicine

基　　金：陕西省自然科学基金(编号:201704A134)。

摘　　要：目的研究维生素D缺乏饮食对链霉素诱导建立的糖尿病小鼠骨缺损修复及骨缺损段Ⅱ型胶原蛋白(ColⅡ)、骨钙素、过氧化物酶体增殖物激活受体(PPAR-γ)和激活蛋白2(AP-2)表达的影响。方法选取30只C54BL6雄性4~5周龄小鼠,按照随机数字表法分为3组,对照组、模型组和VD缺乏组,每组10只。对照组小鼠正常喂养,模型组和VD缺乏组小鼠通过腹腔注射链霉素建立1型糖尿病模型,并且模型组小鼠正常喂养,而VD缺乏组小鼠则给予维生素D缺乏喂养。糖尿病模型建立4周后,通过股骨穿孔建立骨缺损模型。CT扫描观察骨缺损修复和测定骨密度,试剂盒法测定血清25(OH)D3、Ca、P、甲状旁腺素(PTH)以及骨特异性碱性磷酸酶(BAP),定量聚合酶链式反应法测定骨缺损段ColⅡ、骨钙素、PPAR-γ和AP-2 mRNA表达。结果与对照组相比,模型组和VD缺乏组小鼠体重显著下降,而血糖显著上升,差异均有统计学意义(P<0.05),模型组和VD缺乏组小鼠体重与血糖比较,差异均无统计学意义(P>0.05)。与对照组相比,模型组和VD缺乏组小鼠骨缺损面积显著增加,而总体骨密度、皮质骨密度和松质骨密度均显著降低,差异均有统计学意义(P<0.05);与模型组相比,VD缺乏组小鼠骨缺损面积显著增加,而总体骨密度、皮质骨密度和松质骨密度均显著降低,差异均有统计学意义(P<0.05)。与对照组相比,模型组和VD缺乏组小鼠血清Ca、P和PTH浓度均无显著变化(P>0.05),而血清25(OH)D3、BAP浓度以及骨缺损段ColⅡ、骨钙素、PPAR-γ和AP-2 mRNA表达显著降低,差异均有统计学意义(P<0.05);与模型组相比,VD缺乏组小鼠血清25(OH)D3、BAP浓度以及骨缺损段ColⅡ、骨钙素、PPAR-γ和AP-2 mRNA表达更低,差异均有统计学意义(P<0.05)。结论维生素D缺乏引起1型糖尿病小鼠骨密度降低,延缓其骨缺损后修复速度,这可能与维生素D缺乏抑制骨缺损段ColⅡ、骨钙素、PPAR-γ和AP-2 mObjective To study the effect of vitamin D-deficient diet on bone defect repair and the expression of type Ⅱ collagen(ColⅡ),osteocalcin,peroxisome proliferater activated receptor-γ(PPAR-γ)and activator protein-2(AP-2)in diabetic mice induced by streptomycin.Methods A total of 30 C54BL6 male mice aged 4 to 5 weeks were selected and divided into 3 groups according to the random number table method,the control group,the model group and the VD deficiency group,10 mice in each group.The mice in the control group were fed normally,the mice in the model group and the VD deficiency group were given intraperitoneal injection of streptomycin to establish a type Ⅰ diabetes model,and the mice in the model group were fed normally,while the mice in the VD deficiency group were given vitamin D deficiency feed.Four weeks after the establishment of the diabetes model,a bone defect model was established through femoral perforation.qCT scan to observe bone defect repair and determination of bone density,kit method to determine serum 25(OH)D3,Ca,P,parathyroid hormone(PTH)and bone-specific alkaline phosphatase(BAP),qPCR method to determine bone defect Segment ColⅡ,osteocalcin,PPAR-γand AP-2 mRNA expression.Results Compared with the control group,the body weight of the model group and the VD group decreased significantly,the differences were statistically significant(P<0.05),while the serum increased significantly,the differences were statistically significant(P<0.05).There was no statistically significant difference between the model group and the VD group(P>0.05).Compared with the control group,the bone defect area of mice in the model group and the VD deficiency group increased significantly,while the overall bone density,cortical bone density and cancellous bone density decreased significantly,and the differences were statistically significant(P<0.05);and compared with the model group,the bone defect area of mice in the VD deficient group increased significantly,while the overall bone density,cortical bone density and c

关 键 词：小鼠 糖尿病 维生素D 骨缺损 骨修复 

分 类 号：R587.1[医药卫生—内分泌]