跌打通痹膏对兔膝骨关节炎关节软骨MMP-13、Ⅱ型胶原mRNA表达的影响

摘要

目的：观察跌打通痹膏对兔膝骨性关节炎关节软骨基质金属蛋白酶-13（MMP-13）、Ⅱ型胶原mRNA （COL-Ⅱ mRNA）表达的影响。方法选用65只新西兰兔随机分成正常对照组、假手术组、模型组、跌打通痹膏组、骨通贴组，每组13只。模型组、跌打通痹膏组、骨通贴组采用改良Hulth造模法，正常组、假手术组不予处理，模型组、跌打通痹膏组、骨痛贴组分别用胶带、跌打通痹膏、骨痛贴膏贴敷4周，观察治疗后各组实验兔关节软骨改变情况，并检测关节软骨中 MMP-13、COL-Ⅱ mRNA的表达。结果（1）组织学关节软骨评分：跌打通痹膏组评分较模型组低（P<0.05）。（2）MMP-13mRNA检测：模型组MMP-13表达较正常对照组显著提高（P<0.01)，跌打通痹膏组MMP-13 mRNA表达较模型组降低（P<0.01)。（3）COL-ⅡmRNA检测：跌打通痹膏组COL-Ⅱ表达较模型组升高（P<0.01）。结论跌打通痹膏能通过降低Ⅱ型胶原降解，抑制MMP-13 mRNA表达，从而有效保护膝骨关节炎模型兔关节软骨，延缓关节软骨退变。%Objective To observe the effects of Dieda Tongbi emplastrum on MMP-13 (matrix metalloproteinase-13), COL-II mRNA expression in the knee osteoarthritis model rabbits. Methods The 65 healthy New Zealand rabbits were randomly divided into normal control group, sham-operation group, modeling group, Dieda Tongbi emplastrum group, Gutong patch group, 13 rabbits in each group. The model group, Dieda Tongbi emplastrum group, Gutong emplastrum group were built by improved Hulth molding method. The normal group and sham-operation group were opened the joint cavities without any treatment. The model group, Dieda Tongbi emplastrumand and Gutong patch group were treated with adhesive tape, Dieda Tongbi emplastrumand and Gutongtie for 4 weeks, respectively. The changes of joint cartilage in all model rabbits were observed, and the expressions of MMP-13 and COL-ⅡmRNA in joint cartilage were detected. Results (1) The histologic articular cartilage score of Dieda Tongbi emplastrum group was lower than model group (P<0.05). (2) MMP-13 mRNA test: the MMP-13 expression in model group was increased than that in normal control group (P<0.01). The MMP-13 mRNA expression of Dieda Tongbi emplastrum group were lower than that in model group (P<0.01). (3) COL-ⅡmRNA test: the expression of COL-Ⅱ in Dieda Tongbi emplastrum group was increased than that in model group (P<0.01). Conclusion Dieda Tongbi emplastrum can protect the articular cartilage in knee osteoarthritis model rabbits and delay the course of knee joint degeneration by reducing COL-Ⅱdegradation and inhibiting the expression of MMP-13.