类风湿关节炎,动物模型 z-bo 2020-08-04 638

　　[Modeling method] Experimental animals: Wistar rats, male, 4 weeks. Dissolve SEB in 0.1M PBS solution (1mg/5ml, pH7.2), add 1g carboxymethylcellulose and mix well to form a paste. On the 1st and 7th days of the experiment, 0.5 mg and 0.2 mg of emulsified type II collagen were injected subcutaneously into the back and tail of the rats to immunize the rats to create the basis of collagen-induced arthritis model. At the same time, from day 1 to day 9, artificial wind-cooled and humid environment and SEB outer coating were used to induce wind-cold eczema arthralgia syndrome. The method is to stimulate the artificial wind cold and wet once a day. Each time lasts about 1 hour, and the stimulation conditions are as follows. The wind speed is 18m/s. The relative humidity is 100%, the temperature is 7-10°C, and the co-stimulation is 9 days. On days 7-9, evenly apply cellulose paste to the rats and apply them under the ankle joints of the two hind limbs. Each rat has 30 μl (containing 5 μg SEB) and 10 μg SEB on one side. stimulate. Testing method: The typical testing starts on the 10th day, including continuous observation of the joint inflammation score, the surface temperature of the hind limbs and the sufficient amount. On the 30th day, the hind limbs can be X-ray photographed, and the radionuclide 99mTc-MDPECT can also be used for inflammation tracer imaging.

　　[Characteristics of the model] Compared with the simple model of arthritis induced by cold/humidity stimulated collagen, the joint inflammation score, the degree of inflammatory cell infiltration of the joint synovium and the degree of cartilage erosion of this model are respectively when the surface temperature decreases , It increases. The serum rheumatoid factor level was significantly increased, but the triiodothyroxine (T3) content decreased.

　　[Evaluation and application of the model] So far, people have always believed that the joint pain syndrome caused by rheumatism or rheumatic fever is a simple climatic condition, but in this model, a simple artificial air-cooled humidity is used climate. It has been confirmed that this condition cannot aggravate the inflammation of the rat joints. Only when the weather conditions of wind and humidity and external sources of infection or metabolites of infectious agents (such as SEB) work together, joint inflammation will increase. The development of collagen-induced arthritis is related to the genetic background of the rat strain. At the same time, the cold environment obviously stimulates the secretion of serum estradiol in female rats and inhibits inflammation, making female rats unsuitable for simulating wind, cold and wet arthritis. The judgment of rheumatic arthralgia syndrome cannot completely rely on artificial climate simulation, and the surface temperature of inflamed joints is an important indicator. However, the surface temperature of acutely inflamed joints is still higher than that of normal joints. The articular surface temperature of the rheumatoid arthritis model mice is lower than that of the collagen-induced arthritis model, but the degree of inflammation is similar. Better indicators are needed to determine the type of syndrome. This model can be used to study the etiology and etiology of traditional Chinese medicine arthralgia syndrome, and to study the pharmacological and pharmacological effects of rheumatoid arthritis with cold-damp syndrome.

　　In addition, by controlling the temperature of the artificial environment at 36-38°C, we can create a model of rheumatoid arthritis joint syndrome.