拉应力导致关节软骨Ⅰ型胶原蛋白表达的动物实验研究

发布时间：2019-07-03 13:34

【摘要】：目的:检验软骨损伤后局部是否可以产生较大的拉应力,在拉应力的作用下软骨细胞会发生表型变化,由分泌大量的II型胶原蛋白及蛋白聚糖转为大量分泌I型胶原蛋白。方法:运用有限元模拟软骨裂纹型损伤周围的拉应力分布,手术方法是在15只4月龄的新西兰大兔膝关节软骨制作相似的软骨损伤,分别在2、6、20周处死动物,免疫组化法检测软骨损伤周围的I、II型胶原蛋白的表达,番红O-快绿法检测损伤周围的蛋白聚糖的表达情况。结果:有限元模拟发现软骨裂纹型损伤周围可产生拉应力,且拉应力的大小与裂纹的角度有关,在软骨表面呈45°的裂纹局部最大拉应力达到0.59 MPa,而90°裂纹则无拉应力产生。2、6、20周45°裂纹周围I型胶原蛋白免疫组化结果分别为:0.13±0.07、0.18±0.05、0.19±0.09(平均光密度值),P0.05。90°裂纹则未见明显的I型胶原蛋白产生。此外,两种角度的裂纹周围II型胶原蛋白及蛋白聚糖未见明显变化。结论:一种新的理论证实软骨损伤周围出现的拉应力可导致局部I型胶原蛋白的分布增加,从而诱导软骨发生退变。在软骨损伤治疗过程中若能避免这种拉应力,可能会延缓甚至终止软骨的退变过程,可以为OA(骨性关节炎)的临床治疗与预后提供参考。
[Abstract]:Aim: to investigate whether the local tensile stress can be produced after cartilage injury, and the phenotypic changes of cartilage cells will occur under the action of tensile stress, from secreting a large amount of type II collagen and proteoglycan to secreting type I collagen. Methods: finite element method was used to simulate the tensile stress distribution around cartilage crack type injury. similar cartilage injury was made in knee cartilage of 15 4-month-old New Zealand rabbits. The animals were killed at 2, 6 and 20 weeks, respectively. the expression of type I and II collagen around cartilage injury was detected by immunohistochemistry, and the expression of proteoglycan was detected by red O-fast green method. Results: finite element simulation showed that tensile stress could be produced around cartilage crack type injury, and the tensile stress was related to the angle of crack. The local maximum tensile stress of 45 掳crack on cartilage surface was 0.59 MPa, while 90 掳crack had no tensile stress. 2, the results of type I collagen around 45 掳crack at 20 weeks were 0.13 卤0.07, 0.18 卤0.05, 0.19 卤0.09 (mean optical density), respectively. P0.05.90 掳crack showed no obvious type I collagen production. In addition, there was no significant change in type II collagen and proteoglycan around the cracks at the two angles. Conclusion: a new theory confirms that the tensile stress around cartilage injury can increase the distribution of type I collagen and induce cartilage degeneration. If this tensile stress can be avoided in the treatment of cartilage injury, it may delay or even terminate the degeneration of cartilage, which can provide a reference for the clinical treatment and prognosis of OA (osteoarthritis).
【学位授予单位】：苏州大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：R684

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