中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2013年
28期
5133-5138
,共6页
组织构建%软骨组织构建%缺血再灌注%股骨头骺%髋关节%关节软骨%细胞凋亡%软骨细胞%动物模型
組織構建%軟骨組織構建%缺血再灌註%股骨頭骺%髖關節%關節軟骨%細胞凋亡%軟骨細胞%動物模型
조직구건%연골조직구건%결혈재관주%고골두후%관관절%관절연골%세포조망%연골세포%동물모형
tissue construction%cartilage tissue construction%ischemia/reperfusion%femoral head epiphyses%hip joint%articular cartilage%apoptosis%chondrocyte%animal model
背景：缺血再灌注后可以引起关节软骨的退行性变化，但其中具体机制尚无公识。目的：观察发育期髋关节股骨头骺关节软骨及缺血再灌注后关节软骨的退行性变化及其细胞凋亡现象。方法：80只 SD 大鼠随机分为2组，缺血再灌注组建立髋关节缺血再灌注实验动物模型，假手术组开腹暴露腹主动脉5 min 常规关腹。于模型建立后6 h，12 h，24 h，48 h，5 d，2周，4周不同时点对股骨头骺关节软骨进行光镜病理形态学观察，同时对标本进行 TUNEL 法检测股骨头骺关节软骨细胞凋亡现象。结果与结论：缺血再灌注组术后光镜观察到软骨细胞变性、减少、基质可见局限性纤维化等关节软骨退行变化，两组 TUNEL 法检测均观察到关节软骨细胞的凋亡现象，假手术组偶见有散在分布5个以下的软骨细胞凋亡，缺血再灌注组观察到48 h 可见10-30个软骨细胞发生凋亡。结果提示，缺血再灌注对髋关节股骨头骺关节软骨可引起退行性改变，发育期髋关节缺血再灌注后关节软骨的细胞凋亡可能参与关节软骨的损害，抑制关节软骨的细胞凋亡可能有助于防治早发的骨关节炎。
揹景：缺血再灌註後可以引起關節軟骨的退行性變化，但其中具體機製尚無公識。目的：觀察髮育期髖關節股骨頭骺關節軟骨及缺血再灌註後關節軟骨的退行性變化及其細胞凋亡現象。方法：80隻 SD 大鼠隨機分為2組，缺血再灌註組建立髖關節缺血再灌註實驗動物模型，假手術組開腹暴露腹主動脈5 min 常規關腹。于模型建立後6 h，12 h，24 h，48 h，5 d，2週，4週不同時點對股骨頭骺關節軟骨進行光鏡病理形態學觀察，同時對標本進行 TUNEL 法檢測股骨頭骺關節軟骨細胞凋亡現象。結果與結論：缺血再灌註組術後光鏡觀察到軟骨細胞變性、減少、基質可見跼限性纖維化等關節軟骨退行變化，兩組 TUNEL 法檢測均觀察到關節軟骨細胞的凋亡現象，假手術組偶見有散在分佈5箇以下的軟骨細胞凋亡，缺血再灌註組觀察到48 h 可見10-30箇軟骨細胞髮生凋亡。結果提示，缺血再灌註對髖關節股骨頭骺關節軟骨可引起退行性改變，髮育期髖關節缺血再灌註後關節軟骨的細胞凋亡可能參與關節軟骨的損害，抑製關節軟骨的細胞凋亡可能有助于防治早髮的骨關節炎。
배경：결혈재관주후가이인기관절연골적퇴행성변화，단기중구체궤제상무공식。목적：관찰발육기관관절고골두후관절연골급결혈재관주후관절연골적퇴행성변화급기세포조망현상。방법：80지 SD 대서수궤분위2조，결혈재관주조건립관관절결혈재관주실험동물모형，가수술조개복폭로복주동맥5 min 상규관복。우모형건립후6 h，12 h，24 h，48 h，5 d，2주，4주불동시점대고골두후관절연골진행광경병리형태학관찰，동시대표본진행 TUNEL 법검측고골두후관절연골세포조망현상。결과여결론：결혈재관주조술후광경관찰도연골세포변성、감소、기질가견국한성섬유화등관절연골퇴행변화，량조 TUNEL 법검측균관찰도관절연골세포적조망현상，가수술조우견유산재분포5개이하적연골세포조망，결혈재관주조관찰도48 h 가견10-30개연골세포발생조망。결과제시，결혈재관주대관관절고골두후관절연골가인기퇴행성개변，발육기관관절결혈재관주후관절연골적세포조망가능삼여관절연골적손해，억제관절연골적세포조망가능유조우방치조발적골관절염。
BACKGROUND: Ischemia/reperfusion can induce degenerative alterations in articular cartilage. However, the precise mechanism remains poorly understood. OBJECTIVE: To observe the morphological changes and the apoptosis of articular cartilage of femoral head epiphyses with ischemia/reperfusion. METHODS: A total of 80 Sprague-Dawley rats were randomly assigned to two groups: ischemia/reperfusion (model of ischemia/reperfusion in hip joint) and sham-surgery (exposure of abdominal aorta for 5 minutes) groups, with 40 animals in each group. Articular cartilages of femoral head epiphysis were col ected in 6, 12, 24, and 48 hours, 5 days, and 2 and 4 weeks after operation. Morphology of articular cartilage of femoral head epiphyses was examined by light microscope, and cel apoptosis was detected by TUNEL method. RESULTS AND CONCLUSION: Light microscopy showed chondrocytes degeneration and reduction, as wel as fibrosis in matrix of cartilage in the ischemia/reperfusion group. Chondrocyte apoptosis was observed in both groups by TUNEL. Several apoptotic cells, less than five, were observed in the sham-surgery, while 10-30 apoptotic cells were found in ischemia/reperfusion group at 48 hours. Results indicated that ischemia/reperfusion can induce degenerative changes in articular cartilage of femoral head epiphyses, and cel apoptosis in developing hip joint may participate in damage of articular cartilage. Inhibition of chondrocyte apoptosis in articular cartilage may be useful for the prevention and cure of early osteoarthritis.
