ATP6i基因干扰治疗大鼠激素性股骨头坏死塌陷的生物力学研究  

Biomechanics research on ATP6i gene-interference treating steroid-induced necrosis of the femoral heads in rats

作　　者：童培建[1] 杜文喜[1] 陈欢欢[2] 

机构地区：[1]浙江中医药大学附属第一医院骨伤科,杭州310006 [2]浙江中医药大学第一临床医学院

出　　处：《中华骨科杂志》2012年第2期179-184,共6页Chinese Journal of Orthopaedics

摘　　要：目的 探讨ATP6i基因干扰治疗大鼠激素性股骨头坏死塌陷的生物力学作用机制.方法 雄性SD大鼠40只,随机分为空白对照组、实验对照组、ATP6i SiRNA（＋）慢病毒组及ATP6i SiRNA（＋）慢病毒组,每组10只.后三组应用大肠杆菌内毒素联合激素注射12周构建激素性股骨头坏死塌陷大鼠模型.建模后取双侧股骨髁间窝入路,钻孔达股骨颈下,ATP6i SiRNA（＋）慢病毒组及ATP6i SiRNA（＋）慢病毒组予以ATP6i SiRNA转染干扰ATP6i基因表达治疗,实验对照组注射等量生理盐水.1个月后取大鼠右侧股骨头行生物力学检测,测量各组股骨头软骨下骨的载荷、应力强度、弹性模量及轴向刚度；取左侧股骨头行病理组织学检查.结果 ATP6i SiRNA（＋）慢病毒组的载荷、应力强度、弹性模量及轴向刚度分别为（307.01±27.34）N、（60.44±5.38）MPa、（125.29±11.16）MPa、（162.42±14.45）N/mm,高于ATP6i SiRNA（＋）慢病毒组及实验对照组（P＜0.05）.与ATP6i SiRNA（＋）慢病毒组及实验对照组相比,镜下观察ATP6i SiRNA（＋）慢病毒组的股骨头软骨下骨骨小梁明显增粗,而骨骺线变性、坏死及破坏情况无差异.结论 ATP6i基因干扰治疗大鼠激素性股骨头坏死塌陷能明显抑制破骨细胞的泌酸活性,改善股骨头的生物力学性能.Objective To explore the biomechanics mechanism of ATP6i gene-interference treating steroid-induced necrosis of the femoral heads（SINFH）in rats.Methods Forty SD rats were randomly assigned to four groups：blank control group,experimental control group,ATP6i SiRNA（＋）group and ATP6i SiRNA（-）group,10 rats in each group.We established rat models of SINFH by injecting Escherichia Coli Endotoxin and prednisolone for 12 weeks,then cut along the inner side of the patella for about 1 cm and turn the patellar outside of the both knees of the experimental control group,the ATP6i SiRNA（＋）group and the ATP6i SiRNA（-）group,and drill from the intercondylar until the femoral neck.Rats were treated by transfecting ATP6i small interference RNA（ATP6i SiRNA）into the osteoclasts of the femoral heads to interference the expression of ATP6i SiRNA（＋）,or by the ATP6i SiRNA（-）and same amount of saline.One month later,test the ＂load＂,＂stress＂,＂modulus of elasticity＂,and ＂axial stiffness＂ of the right femoral heads of all four groups,and at the same time take the left femoral heads of all four groups for pathological study.Results The ＂load＂,＂stress＂,＂modulus of elasticity＂,and ＂axial stiffness＂ of the ATP6i SiRNA（＋）group were（307.01±27.34）N,（60.44±5.38）MPa,（125.29±11.16）MPa,（162.42±14.45）N/mm,respectively,which were much greater than the ATP6i SiRNA（-）group and the experimental control group（P〈0.05）.In the pathological studies,we found that the trabecula of the femoral heads of the ATP6i SiRNA（＋）group was much thicker than the ATP6i SiRNA（-）group and the experimental control group,but the degeneration,necrosis and breakage of the osteoepiphysis in each group had no statistically significant differences.Conclusion ATP6i gene-interference can inhibit the acid-secreting function of osteoclasts and improve the biomechanical property of the femoral heads of rats in treating the SINFH.

关 键 词：股骨头坏死 基因疗法 生物力学 

分 类 号：R681.8[医药卫生—骨科学]