Prophylactic Administration Of All-Trans Retinoic Acid Reduces Inflammation In Rats With Rheumatoid Arthritis Model
Keywords
Rheumatoid Arthritis, Collagen-Induced Arthritis, All-Trans Retinoic Acid
Abstract
Objective To explore the effect of all-trans retinoic acid (ATRA) on the joint tissue structure, expression levels of related inflammatory cytokines in serum, and cartilage in the rat model of rheumatoid arthritis (CIA) induced by type II collagen (C¢ò) during arthritis formation. Effects on expression levels of damage-related proteins. Methods Female Wistar rats aged 6 to 8 weeks were randomly divided into blank control group, solvent control group, and ATRA dosage groups. Rats in the solvent control group and ATRA dosage groups were intradermally injected with C¢ò and incomplete Freund’s adjuvant in their tails. To induce rheumatoid arthritis, the rats in the blank control group were given an equal amount of normal saline in the same way. Starting from the second day of the initial immunization, rats in each dose group of ATRA were intraperitoneally injected with different doses of ATRA oil (0.05, 0.5, 5 mg/kg), 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. Normal saline, 3 times a week for 3 weeks. The effects of ATRA on arthritis index (AI) scores, pathological morphology of knee and ankle joints, expression levels of related inflammatory cytokines in serum and expression levels of cartilage damage-related proteins in rats were observed. Results From 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 values of the solvent control group tended to be stable, and the AI values of each dose group of ATRA showed an upward trend. , and lower than that in the solvent control group (P<0.05); pathological sections of the knee and ankle joints showed that the ankle joint structures of each dose group of ATRA and the solvent control group were severely disordered, but the difference in semi-quantitative scores of joint damage between the groups was not statistically significant ( P>0.05); In addition, compared with the vehicle control group, the secretion of interleukin-17A (IL-17A) and tumor necrosis factor-¦Á (TNF-¦Á) in each dose group of ATRA was reduced (P<0.05), and the secretion of interleukin-10 (IL -10) Increased secretion (P<0.05); the expression of ADAMTS-4 and MMP-3 in the knee joint was down-regulated (P<0.05), and the expression of other cartilage damage-related proteins was different. There is no statistical significance (P>0.05). Conclusion During the formation phase of collagen-induced arthritis, ATRA can inhibit the secretion of pro-inflammatory factors such as TNF-¦Á and IL-17A, promote the secretion of IL-10, and thereby reduce the inflammatory response in CIA rats during the formation phase of arthritis. This shows that ATRA can delay the progression of the disease during the formation stage of arthritis, and its mechanism of action may be related to correcting the Th1/Th2 and Th17/Treg imbalance.
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