中文摘要：

目的：探讨NF-κB信号通路在压力调控BMSCs/PRF双膜结构修复兔髁突软骨缺损中的作用。方法：取3~4月龄雄性新西兰兔30只,分离、培养骨髓间充质干细胞并制备成细胞膜片,抽取自体兔动脉血制备PRF,将二者复合制备BMSCs/PRF双膜结构。在所有实验动物双侧髁突作直径3 mm的缺损,制备髁突软骨缺损模型;将实验动物随机分为5组（n=6）,A组：即空白对照组,缺损处不充填;B组：双膜结构充填缺损;C组：压力预调双膜结构后充填缺损;D组：NF-κB抑制剂（PDTC）预处理双膜结构后充填缺损;E组：压力预调加抑制剂预处理双膜结构充填缺损。分别于术后2、4、8周取材,HE染色观察缺损修复情况,Real-time PCR方法检测I-κB、P-65和成软骨相关基因Aggrecan、Sox-9的表达水平,并进行统计分析。结果：C组新生髁突软骨组织中NF-κB各信号分子及成软骨相关基因的表达水平均明显高于相同时间取材的其他各组（P〈0.05）,其缺损修复的效果也最好;D组、E组各时间点的NF-κB信号通路相关信号分子及成软骨相关基因表达水平均明显低于A、B、C组（P〈0.05）。结论：BMSCs/PRF双膜结构能明显促进髁突软骨缺损的修复,以压力预调的双膜结构修复效果尤为显著;NF-κB参与了体内压力促双膜结构合成软骨的过程。

英文摘要：

AIM：To investigate the role of NF-κB signaling pathway in condylar cartilage defect repair by pressure-regulated BMSCs/PRF in rabbits.METHODS：Bone marrow mesenchymal stem cells （BMSCs）were cultured from thirty 3 -4 m old New Zealand rabbits and prepared into cell sheets.Platelet-rich fibrin （PRF）were prepared from the arterial blood of the same rabbit.BMSCs/PRF construct was made.Defects of 3 mm in diameter were made on bilat-eral condylar cartilage of the rabbits.The animals were divided into 5 groups （n =6）and the defects were repaired with BMSCs/PRF construct,pressure-regulated BMSCs/PRF,PDTC-pretreated BMSCs/PRF and PDTC-pretreated pressure-regulated BMSCs/PRF,respectively.Animals without treatment served as the controls.2,4 and 8 weeks after opera-tion,the animals were sacrificed and the condylar cartilage were taken.HE staining was used to observe the defect re-pair.I-κB,p-65,aggrecan and Sox-9 mRNA expression was determined by real-time PCR.RESULTS：Pressure-reg-ulated BMSCs/PRF group showed significantly better tissue healing and higher expression of I-κB,p-65,Aggrecan and Sox-9 than the other groups （P〈0.05）.PDTC treatment significantly reduced I-κB,p-65,Aggrecan and Sox-9 ex-pression （P 〈0.05）.Furthermore,PDTC-treated groups showed reduced defect repair effect and the expvession of I-κB,p-65,aggrecan and Sox-9.CONCLUSION：Pressure-regulated BMSCs/PRF may promote condylar cartilage defect repair.NF-κB signaling pathway is involved in the repair of condylar cartilage defects.