目的观察不同浓度臭氧(O3)对类风湿关节炎(RA)大鼠体内TNF-α、TNFRⅠ和TNFRⅡ的影响,阐述O3治疗类风湿关节炎的机理。方法健康雄性Wistar大鼠48只,采用随机数字表法分为CON组、RA组、O2组、O3-10组、O3-20组、O3-30组、O3-40组、O3-50组,每组6只。除空白对照组外,采用注射弗氏完全佐剂乳化的牛Ⅱ型胶原蛋白的方法建立大鼠RA模型。造模后21d,根据分组关节内注射纯氧和浓度分别为10、20、30、40、50μg/ml的O3各1ml,每周1次,共注射3周。治疗前后测量双后肢足爪厚度。治疗结束后1周,检测大鼠血清和滑膜TNF-α、TNFRⅠ和TNFRⅡ的含量。结果治疗结束后,O3-40组大鼠足爪厚度减小,与RA组相比差异有统计学意义(P<0.01)。RA组、O2组、及O3治疗各组血清中TNF-α、TNFRⅠ、TNFRⅡ含量差异无统计学意义(P>0.05)。与RA组相比,O3-40组、O3-50组大鼠滑膜TNF-α、TNFⅡ含量降低,差异有统计学意义(P<0.01)。与RA组相比,O3-40组大鼠滑膜TNFRⅠ含量升高,差异有统计学意义(P<0.05)。结论关节内注射O3可减轻RA大鼠的关节肿胀,浓度为40μg/ml的O3最为明显,作用机制和O3可以降低滑膜内TNF-α、TNFRⅡ的活性,上调TNFRⅠ的表达有关。 Objective To observe the effects of different concentrations of ozone (O3) on TNF-α, TNFRⅠ and TNFRⅡ in rheumatoid arthritis (RA) rats and to elucidate the mechanism of O3 treatment of rheumatoid arthritis. Methods Forty-eight healthy male Wistar rats were randomly divided into CON group, RA group, O2 group, O3-10 group, O3-20 group, O3-30 group, O3-40 group, O3-50 group, 6 per group In addition to the blank control group, rat model of RA was established by injection of cow’s collagen type Ⅱ emulsified with Freund’s complete adjuvant. 21d after modeling, according to intra-articular injection of pure oxygen and concentrations of 10,20,30,40,50μg / ml of O3 each 1ml, once a week for a total of 3 weeks. The thickness of both hind paws was measured before and after treatment. One week after the end of treatment, the contents of TNF-α, TNFRⅠ and TNFRⅡ in rat serum and synovium were detected. Results At the end of treatment, the paw thickness of O3-40 rats decreased, which was significantly different from that of RA rats (P <0.01). There was no significant difference in the levels of TNF-α, TNFRⅠ, TNFRⅡ between RA, O 2 and O 3 groups (P> 0.05). Compared with RA group, the content of TNF-α and TNFⅡ in synovium of O3-40 group and O3-50 group decreased significantly, with statistical significance (P <0.01). Compared with RA group, the content of TNFR Ⅰ in synovial membrane of O3-40 group increased significantly, with statistical significance (P <0.05). Conclusion Intra-articular injection of O3 can reduce joint swelling in RA rats. O3, the concentration of which is 40μg / ml, is most obvious. The mechanism of action is that O3 can reduce the activity of TNF-α and TNFRⅡ in synovium and up-regulate the expression of TNFRⅠ.