Wei Yi-Shan, Li Dai-He, Liu Wan-Lin, Jiang Dian-Ming
Department of Orthopedics, First Affiliated Hospital, Chongqing Medical University Chongqing, China; Department of Orthopedics, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
Department of Orthopedics, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
Balkan Med J. 2016 Nov;33(6):639-644. doi: 10.5152/balkanmedj.2016.150557. Epub 2016 Nov 1.
Developmental dysplasia of the hip (DDH) is an important factor leading to early adult osteoarthritis. Chondrocyte apoptosis has been proven to be an important factor causing osteoarthritis.
The current study aims to explore whether a rabbit model of developmental dysplasia of the hip through cast immobilization in the legs results in chondrocyte apoptosis.
Animal experimentation.
Thirty-two New Zealand white rabbits were divided in three groups with cast plaster-induced dislocation at 2, 4 and 6 weeks. The contralateral hip joint was utilized as a control group. Ten rabbits in each group were sacrificed, and hip specimens were obtained. Bcl-2/Bax, cleaved caspase-3 and cleaved caspase-8 expression were examined by western blot analysis. Chondrocyte apoptosis was analyzed through transmission electron microscopy (TEM) and TUNEL analysis. All experiments were repeated at least three times.
In the experimental group, Bcl-2/Bax, cleaved caspase-3 and cleaved caspase-8 expression were significantly altered. The Bcl-2/Bax ratio decreased with time (all p<0.01), whereas levels of cleaved caspase-3 (p<0.01 and p<0.05) and cleaved caspase-8 (all p<0.05) gradually increased. Chondrocyte apoptosis was observed through transmission electron microscopy (TEM) and TUNEL analysis (p<0.05 at 4 weeks and p<0.01 at 6 weeks).
Prolonged immobilization of rabbit hip caused chondrocyte apoptosis. Reduction of the hip joint may protect chondrocytes from apoptosis, thus preventing secondary osteoarthritis.
发育性髋关节发育不良(DDH)是导致成人早期骨关节炎的重要因素。软骨细胞凋亡已被证明是导致骨关节炎的重要因素。
本研究旨在探讨通过腿部石膏固定建立的发育性髋关节发育不良兔模型是否会导致软骨细胞凋亡。
动物实验。
32只新西兰白兔分为三组,分别在2周、4周和6周时用石膏固定诱导脱位。对侧髋关节作为对照组。每组处死10只兔子,获取髋关节标本。通过蛋白质免疫印迹分析检测Bcl-2/Bax、裂解的半胱天冬酶-3和裂解的半胱天冬酶-8的表达。通过透射电子显微镜(TEM)和TUNEL分析来分析软骨细胞凋亡。所有实验至少重复三次。
在实验组中,Bcl-2/Bax、裂解的半胱天冬酶-3和裂解的半胱天冬酶-8的表达发生了显著变化。Bcl-2/Bax比值随时间下降(所有p<0.01),而裂解的半胱天冬酶-3(p<0.01和p<0.05)和裂解的半胱天冬酶-8(所有p<0.05)的水平逐渐升高。通过透射电子显微镜(TEM)和TUNEL分析观察到软骨细胞凋亡(4周时p<0.05,6周时p<0.01)。
兔髋关节长期固定导致软骨细胞凋亡。髋关节复位可能保护软骨细胞免于凋亡,从而预防继发性骨关节炎。