雪莲注射液对兔膝关节骨性关节炎模型动物血清NO和滑膜组织SOD、MDA的影响

Effect of Xuelian Injection on Nitric Oxide Level in Rabbit Serum of Knee Osteoarthritis and Superoxide Dismutase and Malondialdehyde Level in Rabbit Synovialis of Knee Osteoarthritis

目的:探讨中药雪莲注射液对膝骨性关节炎模型动物氧自由基代谢的影响,,从而探讨雪莲注射液治疗骨关节炎的作用机理。方法:建立骨关节炎动物模型,动物随机分为4组,A组、B组和C组采用Hulth法造模,D组为正常对照组。造模后A组和B组分别注射雪莲注射液和生理盐水,C组空白。分别于术后6、12、24周每组随机取5只兔,采血检测血清一氧化氮(NO,Nitric oxide)含量(硝酸还原酶法),然后用过量麻醉法处死,打开右膝关节腔,取出滑膜,测定滑膜组织中超氧化物歧化酶(SOD,Superoxide dismutase)活性及丙二醛(MDA,Malondialdehyde)含量。结果:(1)除D组以外,各组12周时血清中NO含量均高于6周时;24周时血清中NO含量均高于12周时。NO的表达均逐渐升高,说明NO是参与膝OA发病进程的重要介质,病变的程度越重则含量越高。(2)A组在各时点血清中NO含量均低于B组和C组(P<0.05),说明雪莲注射液能有效抑制骨性关节炎发病病理过程中的一氧化氮的产生。(3)试验显示A组动物滑膜组织中SOD活性显著高于B、C组(P<0.05),而MDA含量显著低于B、C组(P<0.05),B组与C组无显著性差异(P>0.05)。结论:雪莲注射液可有效抑制骨性关节炎发病病理过程中的一氧化氮的产生,显著提高SOD的活性,降低MDA含量,从而起到延缓关节软骨的退变,促进软骨修复的作用。

Objective：To investigate the influence of Xuelian Injection （XLI） on the metabolism of oxygen free radicals so as to explore the mechanism of XLI in treatment of knee osteoarthritis （OA）. Methods： Experimental animals were randomly divided into 4 groups. Except those in the normal control group, rabbit models of knee OA were established by Hulth＇s method. The treatment was as follows： intramuscular XLI in XLI group, normal saline （NS） in control group, nothing in model group and normal control group. The nitric oxide （NO） level in serum and the levels of superoxide dismutase （SOD） and malondialdehyde （MDA） in synovialis were obsered respectively in each group in the 6th, 12th and 24th week. Results： Higher level of NO in the 12th week than in the 6th week was shown in all groups except in normal control group, and the level was higher in the 24th week than in the 12h week in all groups. The level of NO in XLI group was lower than that in NS group and model group （P〈0.05）, with the SOD activity obviously higher and content of MDA lower than those in NS group and model group （P〈0.05）. There was no significant difference between NS group and model group （P〉0.05）. Conclusion：XLI could effectively delay the degeneration of articular cartilage and promote cartilage repair through inhibiting the generation of NO, increasing SOD activity and decreasing MDA content.