牙体牙髓牙周病学杂志
牙體牙髓牙週病學雜誌
아체아수아주병학잡지
CHINESE JOURNAL OF CONSERVATIVE DENTISTRY
2015年
3期
125-132,178
,共9页
石磊%李轶杰%赵萤%赵寅华%邹德慧%张%陈永进
石磊%李軼傑%趙螢%趙寅華%鄒德慧%張%陳永進
석뢰%리질걸%조형%조인화%추덕혜%장%진영진
BMSCs/PRF双膜结构%机械压力%软骨缺损%NF-κB
BMSCs/PRF雙膜結構%機械壓力%軟骨缺損%NF-κB
BMSCs/PRF쌍막결구%궤계압력%연골결손%NF-κB
BMSCs/PRF construct%mechanical pressure%cartilage defect%NF-κB
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。
目的：探討 NF－κB 信號通路在壓力調控 BMSCs／PRF 雙膜結構脩複兔髁突軟骨缺損中的作用。方法：取3～4月齡雄性新西蘭兔30隻，分離、培養骨髓間充質榦細胞併製備成細胞膜片，抽取自體兔動脈血製備 PRF，將二者複閤製備 BMSCs／PRF 雙膜結構。在所有實驗動物雙側髁突作直徑3 mm 的缺損，製備髁突軟骨缺損模型；將實驗動物隨機分為5組（n ＝6），A 組：即空白對照組，缺損處不充填；B 組：雙膜結構充填缺損；C 組：壓力預調雙膜結構後充填缺損；D 組：NF－κB 抑製劑（PDTC）預處理雙膜結構後充填缺損；E 組：壓力預調加抑製劑預處理雙膜結構充填缺損。分彆于術後2、4、8週取材，HE 染色觀察缺損脩複情況，Real－time PCR 方法檢測 I－κB、P－65和成軟骨相關基因 Aggrecan、Sox－9的錶達水平，併進行統計分析。結果：C 組新生髁突軟骨組織中 NF－κB 各信號分子及成軟骨相關基因的錶達水平均明顯高于相同時間取材的其他各組（P ＜0．05），其缺損脩複的效果也最好；D 組、E 組各時間點的 NF－κB 信號通路相關信號分子及成軟骨相關基因錶達水平均明顯低于 A、B、C 組（P ＜0．05）。結論：BMSCs／PRF 雙膜結構能明顯促進髁突軟骨缺損的脩複，以壓力預調的雙膜結構脩複效果尤為顯著；NF－κB 參與瞭體內壓力促雙膜結構閤成軟骨的過程。
목적：탐토 NF－κB 신호통로재압력조공 BMSCs／PRF 쌍막결구수복토과돌연골결손중적작용。방법：취3～4월령웅성신서란토30지，분리、배양골수간충질간세포병제비성세포막편，추취자체토동맥혈제비 PRF，장이자복합제비 BMSCs／PRF 쌍막결구。재소유실험동물쌍측과돌작직경3 mm 적결손，제비과돌연골결손모형；장실험동물수궤분위5조（n ＝6），A 조：즉공백대조조，결손처불충전；B 조：쌍막결구충전결손；C 조：압력예조쌍막결구후충전결손；D 조：NF－κB 억제제（PDTC）예처리쌍막결구후충전결손；E 조：압력예조가억제제예처리쌍막결구충전결손。분별우술후2、4、8주취재，HE 염색관찰결손수복정황，Real－time PCR 방법검측 I－κB、P－65화성연골상관기인 Aggrecan、Sox－9적표체수평，병진행통계분석。결과：C 조신생과돌연골조직중 NF－κB 각신호분자급성연골상관기인적표체수평균명현고우상동시간취재적기타각조（P ＜0．05），기결손수복적효과야최호；D 조、E 조각시간점적 NF－κB 신호통로상관신호분자급성연골상관기인표체수평균명현저우 A、B、C 조（P ＜0．05）。결론：BMSCs／PRF 쌍막결구능명현촉진과돌연골결손적수복，이압력예조적쌍막결구수복효과우위현저；NF－κB 삼여료체내압력촉쌍막결구합성연골적과정。
Abstract] 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.
