脊髓损伤大鼠胫骨骨痂中降钙素基因相关肽的改变

The Change of valcitonin gene-related peptide in tibial fracture callus after spinal cord injury in rats

目的 研究脊髓损伤后大鼠胫骨骨痂中降钙素基因相关肽 (CGRP)的变化及骨痂量的改变。方法 将 10 0只雌性Wistar大鼠随机分为 2组 ,T10～ 11脊髓横断 +右胫骨骨折组和单纯右胫骨骨折组各 5 0只。术后 3、7、14、2 1、2 8d分批处死 ,检查血清碱性磷酸酶 (ALP) ,摄右胫骨X线片行骨痂评分 ,骨痂行苏木精 伊红 (HE)染色和CGRP免疫组织化学染色。结果 脊髓损伤组 3、7d ,ALP均显著升高 (P <0 .0 1) ;脊髓损伤组 2 1、2 8d ,骨痂X线评分高 ;脊髓损伤组早期形成大量纤维骨痂和软骨骨痂 ,骨痂中CGRP免疫阳性神经纤维较少 ,明显增厚的骨膜内层骨祖细胞、幼稚的软骨细胞胞浆内CGRP强阳性表达 ;晚期骨痂中CGRP含量较低 ,编织骨形成少。结论 脊髓损伤后骨痂中CGRP有显著改变 ,并引起骨痂量和质的改变 ,推测神经因素参与调节骨折愈合过程。

Objective\ To study the relationship between the changes of calcitonin gene-related peptide in tibial fracture callus and yield of callus after spinal cord injury in rats. Methods\ One hundred female Wistar rats were randomly divided into spinal cord transection plus tibial fracture group ( n =50) and tibial fracture group ( n =50). The animals were sacrificed in batches 3,7,14,21 and 28 days after operation. The activities of ALP in serum of rats were measured. X-ray plane films of the fractured tibias were taken to evaluate score of callus. Callus were subjected to H-E staining and CGRP immunohistochemical staining. Results\ Activities of ALP in serum of spinal cord injury group were significantly higher than those in tibial fracture group at 3 d and 7 d ( P <0.01). The score of callus in spinal cord injury group was higher than in tibial fracture group at 21 d and 28 d. There were a quantity of fibrous callus and cartilaginous callus formation and few CGRP immunoreactive nerve fibers in callus at early stage after spinal cord injury. Strong immunoreactivity of CGRP was found in osteofenitor cells, chondroblasts, which proliferated in thickened endoperiosteal and amidst callu at 3 d and 7 d in spinal cord injury group. There were few CGRP in callus and a little woven bone callus formation at late stage after spinal injury. Conclusions\ Expression of CGRP in the callus changed greatly, which caused the change of callus yield after spinal cord injury. It was speculated that fracture healing was regulated by neuropeptide.\;