不同时期应用肌肉生长抑制素抑制剂对小鼠骨折的愈合作用

Healing effects of myostatin inhibitors applied at different stages on fractures in mice

背景:近期研究发现肌肉生长抑制素基因敲除小鼠骨骼肌量明显增加,整个骨架的强度和矿化增加,其在骨折修复早期即有表达。目的:检测小鼠腓骨骨折后不同时间应用肌肉生长抑制素对骨折处骨痂量及骨密度的影响。方法:建立小鼠腓骨骨折模型。造模成功的48只小鼠随机均分为仅造模的对照组、造模后不同起始时间腹腔注射相同剂量肌肉生长抑制素抗体的0d组,1,2周组,造模后4周测量骨折处骨痂骨密度,观察细胞肌肉生长抑制素含量变化和肌肉组织变化。结果与结论:造模成功率80%。各组小鼠体质量差异无显著性意义(P>0.05),0d组腓肠肌质量和股痂骨密度明显高于其他3组(P<0.01),其他3组比较差异无显著性意义。与其他3组比较,0d组肌肉细胞组织形态及细胞内肌肉生长抑制素含量也有直观差别。说明造模后及早应用肌肉生长抑制素抑制剂可增加小鼠骨折处骨密度促进骨折处肌肉增生。

BACKGROUND： Recent studies have found that myostatin knockout mice showed a significant increase in muscle mass the intensity and mineralization of the whole skeleton increase as well. Myostatin expression is found in the early stage of fracture repair. OBJECTIVE： To explore the effects of myostatin applied at different stages on the callus amount and bone mineral density of fibula fractures in mice. METHODS： Fibula fracture model was constructed in mice. The 48 model mice were randomly divided into three groups： control group （empty treatment other than model construction）, 0 day group, 1 week group and 2 weeks group （mice in the latter three groups were injected with myostatin antibody of the same dose at different starting times after model construction）. The callus amount of the fractures was measured in the 4th week after model construction. Myostatin content changes and muscle tissue changes were observed. RESULTS AND CONCLUSION： The success rate of model construction was 80%. There was no significant difference in mouse body mass among groups （P 〉 0.05）. The mass of gastrocnemius and the bone mineral density of the callus in the 0 day group were significantly higher than that in the other three groups （P 〈 0.01 ）; there was no significant difference between the other three groups. Compared with the other groups, the tissue morphology of the myostatin content in the 0 day group also had an intuitive difference. These findings indicate that the early application of myostatin inhibitors after model construction can increase the bone mineral density and promote muscle proliferation in mouse fractures.