CAJ | 학술논문

　　背景：课题组前期研究证实，在关节软骨缺损及骨性关节炎的动物模型中，软骨细胞可过度表达基质金属蛋白酶，各种异常刺激均可能打破基质金属蛋白酶与金属蛋白酶组织抑制因子间平衡，从而导致关节软骨细胞外基质退变，软骨细胞功能下降和失调。目的：观察兔关节软骨缺损修复过程中周期性张应力对软骨细胞基质金属蛋白酶表达的影响。方法：建立兔单侧膝关节软骨缺损模型，术后10周分离软骨细胞体外培养，非手术侧软骨细胞为正常组，术侧软骨细胞随机分为高应力组、低应力组及对照组，加载幅度为 sin10%，0.1，1.0，0 Hz 的周期性张应力，于24 h、48 h、1周、2周和4周后 RT-PCR 测定各组基质金属蛋白酶2，3，9，13的表达。结果与结论：加载周期性张应力24 h 后，正常组及对照组间的基质金属蛋白酶2，3，9，13的表达差异有显著性意义(P <0.05)；加载周期性张应力1周、2周及4周后高应力组和低压力组间差异有显著性意义(P <0.05)；同时发现，低应力组中基质金属蛋白酶2，3，9，13的表达持续下降，加载周期性张应力24 h 与4周之间的差异有显著性意义(P <0.05)。可见力学载荷可影响兔关节软骨缺损修复过程中基质金属蛋白酶的表达，在细胞分子水平上，关节软骨缺损病理的发生发展与应力相互影响。
　　배경：과제조전기연구증실，재관절연골결손급골성관절염적동물모형중，연골세포가과도표체기질금속단백매，각충이상자격균가능타파기질금속단백매여금속단백매조직억제인자간평형，종이도치관절연골세포외기질퇴변，연골세포공능하강화실조。목적：관찰토관절연골결손수복과정중주기성장응력대연골세포기질금속단백매표체적영향。방법：건립토단측슬관절연골결손모형，술후10주분리연골세포체외배양，비수술측연골세포위정상조，술측연골세포수궤분위고응력조、저응력조급대조조，가재폭도위 sin10%，0.1，1.0，0 Hz 적주기성장응력，우24 h、48 h、1주、2주화4주후 RT-PCR 측정각조기질금속단백매2，3，9，13적표체。결과여결론：가재주기성장응력24 h 후，정상조급대조조간적기질금속단백매2，3，9，13적표체차이유현저성의의(P <0.05)；가재주기성장응력1주、2주급4주후고응력조화저압력조간차이유현저성의의(P <0.05)；동시발현，저응력조중기질금속단백매2，3，9，13적표체지속하강，가재주기성장응력24 h 여4주지간적차이유현저성의의(P <0.05)。가견역학재하가영향토관절연골결손수복과정중기질금속단백매적표체，재세포분자수평상，관절연골결손병리적발생발전여응력상호영향。
BACKGROUND: Previous studies have confirmed that in the animal models of articular cartilage defects and osteoarthritis, the chondrocytes can overexpress the matrix metal oproteinases. Various abnormal stimuli are likely to break the balance between matrix metal oproteinase and tissue inhibitor of metal oproteinase, thus leading to degeneration of extracel ular matrix of articular cartilage, as wel as the decline and offset of cartilage chondrocytes. OBJECTIVE: To observe the effect of cyclic tensile strain on the expression of matrix metal oproteinases during the repairing process of rabbit articular cartilage defects. METHODS: The animal models of articular cartilage defects were established, and chondrocytes were separated for culture at 10 weeks after operation. The chondrocytes on the non-surgical side were considered as the normal group, and the chondrocytes on the surgical side were randomly divided into high cyclic tensile strain group, low cyclic tensile strains group and control group, and the load amplitude was sin10%. Then 0.1, 1.0 and 0 Hz cyclic tensile strains were loaded respectively. The expressions of matrix metal oproteinases 2, 3, 9 and 13 in each group were detected with reverse transcription-PCR at 24, 48 hours, 1, 2 and 4 weeks after loading cyclic tensile strain. RESULTS AND CONCLUSION: There were significant differences in the expressions of matrix metal oproteinases 2, 3, 9 and 13 at 24 hours after loading cyclic tensile strain between the normal group and the control group (P < 0.05); and there were significant differences in the expressions between the high cyclic tensile strain group and the low cyclic tensile strain group at 1, 2 and 4 weeks after loading cyclic tensile strain (P < 0.05).At the same time, the expressions of matrix metal oproteinases 2, 3, 9 and 13 in the low cyclic tensile strain group were continued to decline, and there were significant differences in the expressions after loading cyclic tensile strain for 24 hours and 4 weeks (P < 0.05). The results indicate that mechanical load can affect the expression of matrix metal oproteinases in the healing process of rabbit articular cartilage defects. In the cel ular and molecular level, the incidence and development of pathological articular cartilage defect and stress should affect each other.