中华创伤骨科杂志
中華創傷骨科雜誌
중화창상골과잡지
CHINESE JOURNAL OF ORTHOPAEDIC TRAUMA
2015年
8期
714-718
,共5页
赵雄%李端%吴子祥%张扬%石磊%雷伟%颉强
趙雄%李耑%吳子祥%張颺%石磊%雷偉%頡彊
조웅%리단%오자상%장양%석뢰%뢰위%힐강
骨折愈合%生物力学%增殖细胞核抗原%血管内皮细胞生长因子
骨摺愈閤%生物力學%增殖細胞覈抗原%血管內皮細胞生長因子
골절유합%생물역학%증식세포핵항원%혈관내피세포생장인자
Fracture healing%Biomechanics%Proliferating cell nuclear antigen%Vascular endothelial growth factors
目的 探讨替米沙坦对小鼠股骨干骨折愈合的影响. 方法 取64只3个月龄雄性BALB/c小鼠,随机分为2组(n=32):实验组小鼠每天饮水中按30 mg/kg加入替米沙坦,对照组给予正常饮水.采用股骨截骨方法建立右股骨干骨折模型,于术后2、5、10周通过X线片、生物力学测试、组织形态学分析比较两组小鼠的骨折愈合情况,通过免疫组织化学方法比较两组小鼠增殖细胞核抗原及血管内皮细胞生长因子阳性表达的差异. 结果 术后2周X线片示实验组小鼠骨痂直径与股骨直径比值(243.7%±38.1%)显著大于对照组(178.2%±24.5%),差异有统计学意义(P<0.05);术后5、10周,两组小鼠骨痂直径与股骨直径比值比较差异均无统计学意义(P>0.05).组织形态学结果进一步支持影像学结果,与对照组比较,实验组小鼠骨形成更加显著.术后2周,实验组小鼠股骨的最大抗扭转力(31.4%±5.1%)和扭转刚度(37.7%±8.6%)均显著大于对照组(16.7%±4.2%、19.5%±7.3%),差异有统计学意义(P<0.05).术后2周,实验组小鼠增殖细胞核抗原阳性表达(53.8%±7.5%)、血管内皮细胞生长因子阳性表达(39.2%±6.8%)均显著高于对照组(36.1%±5.4%、21.3%±4.9%),差异有统计学意义(P<0.05). 结论 替米沙坦可能通过诱导细胞增殖和新生血管形成来促进小鼠股骨干骨折愈合.
目的 探討替米沙坦對小鼠股骨榦骨摺愈閤的影響. 方法 取64隻3箇月齡雄性BALB/c小鼠,隨機分為2組(n=32):實驗組小鼠每天飲水中按30 mg/kg加入替米沙坦,對照組給予正常飲水.採用股骨截骨方法建立右股骨榦骨摺模型,于術後2、5、10週通過X線片、生物力學測試、組織形態學分析比較兩組小鼠的骨摺愈閤情況,通過免疫組織化學方法比較兩組小鼠增殖細胞覈抗原及血管內皮細胞生長因子暘性錶達的差異. 結果 術後2週X線片示實驗組小鼠骨痂直徑與股骨直徑比值(243.7%±38.1%)顯著大于對照組(178.2%±24.5%),差異有統計學意義(P<0.05);術後5、10週,兩組小鼠骨痂直徑與股骨直徑比值比較差異均無統計學意義(P>0.05).組織形態學結果進一步支持影像學結果,與對照組比較,實驗組小鼠骨形成更加顯著.術後2週,實驗組小鼠股骨的最大抗扭轉力(31.4%±5.1%)和扭轉剛度(37.7%±8.6%)均顯著大于對照組(16.7%±4.2%、19.5%±7.3%),差異有統計學意義(P<0.05).術後2週,實驗組小鼠增殖細胞覈抗原暘性錶達(53.8%±7.5%)、血管內皮細胞生長因子暘性錶達(39.2%±6.8%)均顯著高于對照組(36.1%±5.4%、21.3%±4.9%),差異有統計學意義(P<0.05). 結論 替米沙坦可能通過誘導細胞增殖和新生血管形成來促進小鼠股骨榦骨摺愈閤.
목적 탐토체미사탄대소서고골간골절유합적영향. 방법 취64지3개월령웅성BALB/c소서,수궤분위2조(n=32):실험조소서매천음수중안30 mg/kg가입체미사탄,대조조급여정상음수.채용고골절골방법건립우고골간골절모형,우술후2、5、10주통과X선편、생물역학측시、조직형태학분석비교량조소서적골절유합정황,통과면역조직화학방법비교량조소서증식세포핵항원급혈관내피세포생장인자양성표체적차이. 결과 술후2주X선편시실험조소서골가직경여고골직경비치(243.7%±38.1%)현저대우대조조(178.2%±24.5%),차이유통계학의의(P<0.05);술후5、10주,량조소서골가직경여고골직경비치비교차이균무통계학의의(P>0.05).조직형태학결과진일보지지영상학결과,여대조조비교,실험조소서골형성경가현저.술후2주,실험조소서고골적최대항뉴전력(31.4%±5.1%)화뉴전강도(37.7%±8.6%)균현저대우대조조(16.7%±4.2%、19.5%±7.3%),차이유통계학의의(P<0.05).술후2주,실험조소서증식세포핵항원양성표체(53.8%±7.5%)、혈관내피세포생장인자양성표체(39.2%±6.8%)균현저고우대조조(36.1%±5.4%、21.3%±4.9%),차이유통계학의의(P<0.05). 결론 체미사탄가능통과유도세포증식화신생혈관형성래촉진소서고골간골절유합.
Objective To study the effect of telmisartan on healing of femoral shaft fracture in mice.Methods Models of fracture of right femoral shaft were created by femoral osteotomy in 64 mature male BALB/c mice which were randomized into 2 equal groups (n =32).The experimental group was treated with telmisartan (30 mg/kg in drinking water) while the control group only with normal drinking water.Fracture healing was analyzed after 2,5 and 10 weeks postoperatively using X-ray,biomechanical testing,and histomorphometry.Immunohistochemistry was applied to compare the expression of proliferating cell nuclear antigen (PCNA) and vascular endothelial growth factor (VEGF) in the callus between the 2 groups.Results Radiological analysis at 2 weeks postoperation showed the callus diameter in the telmisartan treated animals (243.7 ± 38.1%) was significantly larger than in the vehicle treated controls (178.2 ± 24.5%) (P < 0.05).There were no significant differences in the callus diameter between the 2 groups at 5 or 10 weeks postoperation (P > 0.05).Histomorphometric analyses revealed a significantly increased amount of bone formation in the experimental group compared with the control group.Biomechanical testing further showed significantly greater peak torque at failure (31.4 ± 5.1%) and significantly higher torsional stiffness (37.7 ± 8.6%) in the telmisartan-treated group than those (16.7 ±4.2% and 19.5 ±7.3%,respectively) in the vehicle-treated group after 2 weeks of fracture healing (P > 0.05).There was an increased fraction of PCNA-positive cells (53.8 ±7.5%) and VEGF-positive cells (39.2 ±6.8%) in the telmisartan-treated group compared with the vehicle-treated group (36.1 ± 5.4% and 21.3 ± 4.9%,respectively) after 2weeks of fracture healing (P >0.05).Conclusions Telmisartan can promote healing of femoral shaft fracture,probably by increasing cell proliferation and neovascularization associated with decreased VEGF expression in hypertrophic chondrocytes.