膝骨性关节炎的发病机制及降钙素的治疗作用

Pathogenesis of knee osteoarthritis and therapeupic effect of calcitonin

目的探讨膝骨性关节炎(KOA)的发病机制及降钙素(CT)的治疗作用。方法 36只白兔随机均分为空白对照组(A组)、KOA模型组(B组)、CT 5U.kg-1.d-1治疗组(C组)。20d后处死动物,检测血清及关节液超氧化物歧化酶(SOD)活性及丙二醛(MDA)、一氧化氮(NO)含量,HE染色观察关节软骨病理组织学变化,免疫组织化学染色法检测软骨组织Ⅱ型胶原和基质金属蛋白酶1(MMP-1)蛋白表达情况。结果与A组相比,B组关节软骨损伤加重,Mankin's评分、MDA及NO含量、MMP-1蛋白表达增加(P<0.05),SOD活性及Ⅱ型胶原含量降低(P<0.05);而C组能明显逆转B组上述各观察指标的改变过程(P<0.05)。结论 KOA的发生与机体氧化-抗氧化系统、细胞外基质合成-分解代谢系统的失衡密切相关,且CT对KOA的治疗作用与这两个系统失衡的恢复有关。

Objective To investigate the pathogenesis of knee osteoarthritis（KOA） and the therapeutic efficacy of calcitonin（CT） on KOA. Methods Thirty-six rabbits were equally randomized into three groups of A（normal controls）,B（KOA model） and C（treated with CT 5 U·kg-1·d-1 after establishing KOA model）.The rabbits were sacrificed 20 days later,and the activity of superoxide dismutase（SOD） and content of malondialdehyde（MDA） and nitric oxide（NO） in serum and synovia were measured.The pathohistology change of articular cartilage and the protein expressions of collagen Ⅱ and matrix metalloproteinase-1（MMP-1） in the cartilage tissues were detected by HE staining and immunohistochemistry,respectively. Results Compared with group A,the injury of articular cartilage was more serious,the Mankin＇s score,the content of MDA and NO and the protein expression of MMP-1 were increased（P0.05）,whereas the activity of SOD and the content of collagen Ⅱ were decreased（P0.05） in group B,which were all significantly reversed in group C（P0.05）. Conclusion The imbalance of both oxidation-antioxidation system and synthesis-degradation of cartilage matrix system may play an important role in the development of KOA,and the treatment of CT on KOA is relevant to the recovery of imbalance of these two systems.