卵巢切除股骨骨折大鼠骨愈合中降钙素的作用

背景：降钙素可活化腺苷酸环化酶蛋白激酶A通路及磷脂酶C通路，抑制破骨细胞的活性，可能治疗骨质疏松性骨折。 目的：观察降钙素对去卵巢大鼠股骨骨折愈合的作用。 方法：构建双侧卵巢切除骨质疏松右股骨骨折SD大鼠模型，然后分别皮下注射生理盐水和降钙素(16 IU/kg)，隔日1次，于骨折后3周和6周测量右股骨行骨密度，苏木精-伊红及抗酒石酸酸性磷酸酶染色，骨形态发生蛋白2及血管内皮生长因子免疫组化染色。 结果与结论：骨折后给予降钙素治疗的大鼠抗酒石酸酸性磷酸酶染色阳性细胞积分吸光度值较生理盐水治疗的大鼠显著减少(P < 0.05)。骨折后3周，两组骨折线均较清晰，骨痂体积无明显差别，骨折愈合以软骨内化骨过程为主，骨密度无显著性差异(P > 0.05)。骨折后6周，两组骨折线较模糊，骨痂体积无差别，骨小梁排列较有序，用药组股骨骨密度较对照组升高(P < 0.05)。两组在骨折后3周和6周的骨形态发生蛋白2及血管内皮生长因子差异无显著性意义(P > 0.05)。证实降钙素可以抑制去卵巢大鼠骨折部位破骨细胞活性，但无明显促进大鼠股骨骨折愈合的作用。

Effect of calcitonin on femoral fracture healing in ovariectomized rats

BACKGROUND: Calcitonin can activates adenylyl cyclase protein kinase A pathway and phospholipase C pathway, inhibits activity of osteoclast, may treats osteoporotic fracture. OBJECTIVE: To observe the effect of calcitonin on femoral fracture healing in ovariectomized rats. METHODS: Ovariectomized SD rat right femur fracture model was constructed, normal saline and calcitonin (16 IU/kg) were injected subcutaneously in the neck once per two days, respectively. Right bone mineral density (BMD) was measured at 3 weeks and 6 weeks after fracture, stained with hematoxylin- eosin (HE) and tartrate-resistant acid phosphatase (TRAP) staining, as well as bone morphogenetic protein 2 (BMP-2) and vascular endothelial growth factor (VEGF) immunohistochemistry staining. RESULTS AND CONCLUSION: Tartrate-resistant acid phosphataste positive staining cells integral absorbance values of rats received calcitonin treatment after fracture was decreased significantly compared with rats received saline treatment (P < 0.05). SD rats were randomly divided into ovariectomy + fracture + calcitonin (experimental) group and ovariectomy + fracture + saline (control) group. At 3 weeks after fracture, fracture lines were clearly in both experimental group and control group, there was no significant difference in callus volume; endochondral ossification was dominant in fracture healing, there was no significant difference in BMD (P < 0.05). At 6 weeks after fracture, fracture lines were ambiguous in both experimental group and control group; there was no difference in callus volume, bone trabeculae arranged orderly, BMD of right femur increased significantly in experimental group compared with control group (P < 0.05). There was no significant difference of BMP-2 and VEGF between experimental group and control group at 3 weeks and 6 weeks after fracture (P > 0.05). The results demonstrated that calcitonin can inhibits osteoclast cell at fracture cite in ovariectomized rats, but has no significant effect on the promotion of femoral fracture healing in ovariectomized rats.