摘要
目的:探讨不同干预手段,对骨折大鼠愈合过程中骨折部位CD34、FⅧ-RAg及血管再生通路VEGF/VEGFR-2的影响,为加速骨折愈合提供理论依据。方法:选取80只3月龄SD大鼠,随机分为4组,分别为骨折模型组;骨折+动员剂组;骨折+被动收缩组;骨折+动员剂+被动收缩组。骨折后分别在2、4、6、8周取材,制成脱钙骨切片;免疫组织化学染色方法测试骨折愈合过程骨痂处CD34、FⅧ-RAg及血管再生通路VEGF/VEGFR-2表达。结果:免疫组化结果显示,各干预手段均可增加CD34、FⅧ-RAg、VEGF、VEGFR-2在大鼠骨折部位的表达量。且动员剂+被动收缩组>被动收缩组>动员剂组>模型组。结论:骨骼肌被动收缩和(或)rhG-CSF干预均可促进造血干细胞/内皮祖细胞(HSCs/EPCs)的动员,促进血管再生通路VEGF/VEGFR-2的表达,促进血管再生,且被动收缩协同rhG-CSF动员的双重作用效果更为显著。此方法简单、易行,为骨折病人早期运动康复手段与方法的筛选提供基础理论依据。
Objective : This study explored the effects of different interventions on CD34, FⅧ-RAg and angiogenesis pathway VEGF/VEGFR - 2 in fracture position during the process of fracture healing in rats, in order to provide theoretic basis for fracture healing. Methods: Eighty-three months old SD rats were randomly divided into 4 groups: the fracture model group; fracture combined recruitment group; fracture combined passive contraction group; fracture combined recruitment and passive contraction group. Tissues were collected at 2, 4, 6, 8 weeks respectively and were made of decalcified bone section. The expressions of CD34, FⅧ-RAg and vascular regenera- tion pathway of VEGF/VEGFR - 2 in fracture position were measured by immunohistochemical staining. Results : Immunohistochemieal results showed that all interventions can increase expressions of CD34, FⅧ-RAg, VEGF, VEGFR- 2 in fracture position. And the expressions of these factors in groups were racked from high to low: recruitment combined passive contraction group, passive contraction group, recruitment group, model group. Conclusion: Skeletal muscle passive contraction and/or rhG-CSF can promote recruitment of HSCs/EPCs, can increase the expression of VEGF/VEGFR - 2, and can help vascular regeneration. Passive contraction combined rhG-CSF had most significant effect compared with other interventions. Also this way was simple and doable, and provided theoretic basis for estimate rehabilitation methods in early stage for fracture patients.
出处
《北京体育大学学报》
CSSCI
北大核心
2014年第1期82-87,共6页
Journal of Beijing Sport University
基金
陕西师范大学"211工程"重点建设学科--运动生物学学科建设项目(2010.11)