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目的观察盘状结构域受体2(DDR2)在改良的佐剂诱导性大鼠类风湿关节炎(RA)模型不同病理阶段的表达情况,从蛋白水平揭示DDR2在实验性类风湿关节炎模型的表达规律。方法改良佐剂型大鼠RA模型,以免疫组织化学方法结合激光共聚焦显微镜检测DDR2在不同病理阶段的表达情况;同时利用酶联免疫吸附试验(ELISA)检测大鼠血清中抗Ⅱ型胶原(CⅡ)抗体水平。结果①在本实验条件下可以更好更迅速地建立在临床表现、病理特征和实验室检查都与实际病人非常类似的病理模型。②免疫组织化学显示致敏后第15天即可观察到DDR2的表达,此后,随着时间的推移,后者的表达呈递增趋势,约在免疫后第35天左右DDR2的表达达到高峰期。③免疫荧光组织化学显示免疫后第28天以后即可观察到DDR2的表达开始出现上升趋势,随后的时间里,它的表达呈一个直线上升的趋势,约在35~40d左右达到最高峰,随后开始下降。④ELISA显示,大鼠血清中的抗CⅡ抗体随着免疫时间的推移也呈递增趋势,约在免疫后第40天左右达到峰值,随后开始降低。结论随病情的发展DDR2的表达有时间依赖性,提示后者在RA的发病机制中可能具有重要作用。
Objective To investigate the expression of discoid domain receptor 2 (DDR2) at different pathological stages in a modified adjuvant-induced rat rheumatoid arthritis (RA) model, revealing the role of DDR2 in experimental rheumatoid arthritis model The law of expression. Methods The adjuvant-induced rat model of RA was ameliorated. The expression of DDR2 in different pathological stages was detected by immunohistochemistry and laser confocal microscopy. Meanwhile, the level of anti-type Ⅱ collagen (CⅡ) in rat serum was detected by enzyme linked immunosorbent assay (ELISA) ) Antibody level. Results ① Under this experimental condition, it is possible to establish the pathological model which is very similar to the actual patient in the clinical manifestations, pathological features and laboratory tests. ② Immunohistochemistry showed that DDR2 expression was observed on the 15th day after sensitization. Afterwards, the expression of DDR2 increased gradually with the passage of time. The expression of DDR2 peaked at about the 35th day after immunization. ③ Immunofluorescence histochemistry showed that the expression of DDR2 began to show an upward trend after 28 days after immunization. At a later time, its expression showed a linear upward trend, reaching the peak around 35 ~ 40d, begin descending. ④ELISA showed that the anti-CⅡantibody in serum of rats increased gradually with the passage of time and reached the peak at about the 40th day after immunization, and then began to decrease. Conclusion With the progression of the disease, the expression of DDR2 is time-dependent, suggesting that the latter may play an important role in the pathogenesis of RA.