动物造模,类风湿关节炎模型 z-bio 2023-01-31 481

　　OBJECTIVE: To explore the effect of all-trans retinoic acid (ATRA) on the type II collagen (CII) induced rheumatoid arthritis model (CIA) rat arthritis formation stage joint tissue structure, serum related inflammatory cytokine expression level, and The influence of the expression level of cartilage damage-related proteins.

　　Methods: 6-8 weeks old female Wistar rats were randomly divided into blank control group, solvent control group, and ATRA each dose group. The solvent control group and ATRA each dose group were given intradermal injection of CⅡ and incomplete Freund's Zol at the tail of the rats. To induce rheumatoid arthritis, rats in the blank control group were given the same amount of normal saline in the same way. From the second day of the initial immunization, rats in each ATRA dose group were intraperitoneally injected with different doses (0.05, 0.5, 5 mg/kg) of ATRA oil, the solvent control group was intraperitoneally injected with an equal volume of corn oil, and the blank control group was intraperitoneally injected with an equal volume of corn oil. Normal saline, 3 times a week for 3 consecutive weeks. To observe the effects of ATRA on rat arthritis index (AI) score, histopathological morphology of knee and ankle joints, the expression level of related inflammatory cytokines in serum, and the expression level of cartilage injury-related proteins.

　　Results: Since the 15th day of the initial immunization, the AI values of each dose group of ATRA and the solvent control group were significantly higher than those of the blank control group (P<0.05), the AI value of the solvent control group tended to be stable, and the AI value of each dose group of ATRA increased The trend is lower than that of the solvent control group (P<0.05); the="" pathological="" section="" of="" knee="" and="" ankle="" joint="" can="" be="" atra="" dose="" group="" solvent="" pair="" p="">0.05); in addition, compared with the solvent control group, the ATRA dose group interleukin -17A (IL-17A) and tumor necrosis factor-α (TNF-α) secretion decreased (P<0.05), interleukin-10 (IL-10) secretion increased (P<0.05); unintegrated protein metal in the knee joint The expression of protease (ADAMTS-4) and matrix metalloproteinase (MMP-3) was down-regulated (P<0.05), and="" there="" was="" no="" statistical="" difference="" in="" the="" expression="" of="" other="" cartilage="" damage-related="" proteins="" p="">0.05).

　　Conclusion: During the formation of collagen-induced arthritis, ATRA can inhibit the secretion of TNF-α, IL-17A and other pro-inflammatory factors, and promote the secretion of IL-10, thereby reducing the inflammatory response during the formation of arthritis in CIA rats. This shows that ATRA can delay the progression of the disease during the development of arthritis, and its mechanism of action may be related to the correction of Th1/Th2 and Th17/Treg imbalance.