应用鼠神经生长因子修复周围神经损伤对骨质疏松的影响

背景：神经损伤后骨质疏松症发生机制与其他原因造成的失用性骨质疏松症不完全相同,在其发生发展过程中可能蕴含着更为复杂的因素,除了失去应力刺激外,细胞因子异常、神经功能的异常、激素水平的改变均参与了神经损伤后骨质疏松的发生。目的：通过活体动物实验探讨神经损伤后和骨质疏松的相互关系。方法：雄性SD大鼠随机分为正常对照组和失神经组,失神经组大鼠切断股骨神经造成失神经支配模型,然后分为模型对照组和失神经支配注射鼠神经生长因子组（神经生长因子组）。神经生长因子组在两侧下肢腓肠肌处部位注射鼠神经生长因子0.2 mL,频率1次/d,失神经支配对照组注射同等量生理盐水,正常对照组不做处置。30 d后称质量、取血、处死动物,取股骨进行骨组织计量学检查。结果与结论：失神经支配大鼠注射鼠神经生长因子后,体质量、骨小梁量与模型对照组相比具有明显增加,提示局部予以鼠神经生长因子治疗可明显减轻失神经支配后大鼠骨质疏松的程度,并可减弱因失神经导致的体质量减轻,而各组的血钙磷浓度无明显改变。说明神经性骨质疏松的发生并非源自钙磷流失,而是由骨小梁的结构改变所致,同时外源性鼠神经生长因子在神经性瘫痪后骨质疏松的恢复中具有积极意义。

Effect of mouse nerve growth factor on osteoporosis after peripheral nerve injury

BACKGROUND： Osteoporosis after nerve injury has different pathogenesis from osteoporosis of other causes. A more complex set of factors can be involved in the occurrence and development of osteoporosis after nerve injury In addition to the loss of stress stimulation, cytokines abnormalities, abnormal nerve function and variation of hormone levels are all involved in osteoporosis after nerve injury. OBJECTIVE： To observe the interaction between nerve injury and osteoporosis by using living animal experiments. METHODS： Male Sprague-Dawley rats were randomly divided into normal control and denervation groups. Denervated rat models were caused by cutting off the femoral nerve, and then subdivided into model group and nerve growth factor group. Rats in the nerve growth factor group were subjected to 0.2 ml_ nerve growth factor injection into the gastrocnemius of bilateral lower limbs, once a day; while rats in the model group were subjected to the same volume of saline. No treatment was done in the normal control group. After 30 days, the rats were weighted and blood samples were collected followed by killing, and then the femur bone was taken out for histomorphometry examination.RESULTS AND CONCLUSION： After injection of nerve growth factor, the body mass and trabecular bone volume of rats in the nerve growth factor group was significantly higher than those in the model group, indicating local injection of nerve growth factor could obviously reduce the extent of osteoporosis in denervated rats, and meanwhile weaken the weight loss due to denervation. However, there was no change in blood calcium and phosphorus concentrations in each group. Experimental findings suggest that neurological osteoporosis does not originate from the loss of calcium and phosphorus but by structural changes in the trabecular bone; meanwhile, exogenous mouse nerve growth factor is of positive significance for osteoporosis following after nerve paralysis.