首页> 中文期刊> 《中国康复医学杂志》 >电针对实验性兔膝骨关节炎模型白细胞介素-1β和基质金属蛋白酶-1表达的影响

电针对实验性兔膝骨关节炎模型白细胞介素-1β和基质金属蛋白酶-1表达的影响

         

摘要

目的:观察电针治疗前后兔膝骨关节炎(KOA)模型关节冲洗液中细胞因子白介素-1 β(IL-1 β)和软骨中基质金属蛋白酶-1(MMP-1)表达的变化,探讨电针治疗KOA的作用机制.方法:将30只新西兰大耳兔随机分为正常组、模型组及电针组.正常组为对照组,模型组和电针治疗组采用左膝关节伸直位管型石膏固定6周制作KOA模型,电针治疗组电针治疗14d.分别观察各组兔造模结束和治疗后左膝关节冲洗液中IL-1 β含量变化,治疗后各组兔左股骨内侧髁软骨MMP-1表达的变化.结果:采用放免法行关节冲洗液IL-1 β含量测定,造模结束后正常组与模型组、电针治疗组组间比较,其后两者明显高于前者(P<0.05),治疗结束后模型组、电针治疗组组间比较,前者显著高于后者(P<0.05).治疗结束后软骨免疫组化法MMP-1测定,模型组和电针治疗组的MMP-1阳性率明显高于正常组(P<0.05),且模型组MMP-1阳性率高于电针治疗组(P<0.05).结论:电针能有效治疗KOA,其作用机制可能是电针使KOA关节中细胞因子IL-1 β和软骨中MMP-1的含量减少,从而降低Ⅱ型胶原和蛋白聚糖的降解,促进新的Ⅱ型胶原和蛋白聚糖合成,改善血液循环,促进经气运行,从而有利于关节渗出液吸收,促进软骨的修复.%Objective: To observe the changes of interleukin-1 β (IL-1β) from joint irrigation and matrix metalloproteinase-1 (MMP-1) from cartilage expressed in rabbit's knee osteoarthritis(KOA) model before and after electro-acupuncture (EA) treatment, to explore the mechanism of EA treatment on knee osteoarthritis.rnMethod: Thirty healthy New Zealand big-ear rabbits were randomly divided into normal group, model group and EA group. In the latter two groups left knees were fixed in extension position with plaster cast for 6 weeks to establish KOA models. The EA group was treated for 14d. The changes of content of IL-1β expression in joint irrigation after modeling and treatment and changes of MMP-1 expression in cartilage of left condylus after treatment were observed respectively.rnResult: The radioimmunoassay detection results revealed IL-1 β expression in joint irrigation of model group and EA group after modeling were significantly higher than that of control group (P<0.05), while the IL-1 β expression in model group was significantly higher than that in EA group after treatment (P < 0.05). By immunohisto- chemical detection, the MMP-1 positive rates of model group and EA group were significantly higher than that of control group (P < 0.05), with a higher rate in model group(P<0.05).rnConclusion: EA treatment can effectively improve the rahhit's KOA, the mechanism of which is probably related with IL-1β reduction in joint and MMP-1 decrease in cartilage so as to, prevent the collagen Ⅱ and proteogly-can from degradation, promote new collagen Ⅱ and proteoglycan formation, improve blood and qi circulation, thus promote the absorption of joint exudates and cartilage repair.

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