动物造模,风湿关节炎模型 z-bio 2021-11-05 336

　　OBJECTIVE: To study the effect of all-trans retinoic acid (ATRA) on the joint tissue structure, serum-related inflammatory cytokine expression level and expression of rheumatoid arthritis model (CIA) rats induced by collagen type II (CII) Affect the level of damage-related proteins.

　　Method: 6-8 weeks old female Wistar rats were randomly divided into blank control group, solvent control group and ATRA dose group. Rheumatoid arthritis is not completely caused by intradermal injection of CII into the solvent control group and each dose group of ATRA. Under the induction of adjuvant, rats in the blank control group were given the same amount of normal saline in the same manner. From the second day of the first immunization, rats in each dose group of ATRA were injected intraperitoneally with different doses (0.05, 0.5, 5 mg/kg) of ATRA oil, and the same amount of corn oil was injected intraperitoneally into the solvent Control group. I injected the blank control group with an equal volume of saline intraperitoneally for three consecutive weeks every week, three times a week. To observe the effects of ATRA on the rat arthritis index (AI) score, the histopathological morphology of the knee and ankle joints, the expression levels of related inflammatory cytokines in the serum, and the expression levels of cartilage injury-related proteins.

　　Results: 15 days after the first immunization, the AI value of the ATRA treatment group and the solvent control group was significantly higher than that of the blank control group (P0.05). In addition, the secretion of IL-17A (IL-17A) and tumor necrosis factor-α (TNF-α) in the solvent control group and ATRA dose group decreased (P0.05).

　　Conclusion: During the formation of collagen-induced arthritis, ATRA inhibits the secretion of TNF-α, IL-17A and other pro-inflammatory factors, and promotes the secretion of IL-10, thereby causing inflammation. It can be reduced in CIA rats. This indicates that ATRA can slow down the progression of the disease during the onset of arthritis, and its mechanism of action may be related to the correction of Th1/Th2 and Th17/Treg imbalance.