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Effects and mechanisms of vitamin A and vitamin E on the levels of serum leptin and other related cytokines in rats with rheumatoid arthritis

机译:维生素A和维生素E对类风湿关节炎大鼠血清瘦素及其他相关细胞因子水平的影响及其机制

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摘要

Leptin has been identified as an important cytokine in the inflammatory networks of rheumatoid arthritis (RA). Higher serum leptin levels may accelerate the development of RA. This study aimed to examine the effects of vitamin A (VitA) and vitamin E (VitE) on the levels of leptin and other related experimental and clinical indices, and to explore the mechanisms of these effects through the Janus kinase/signal transducer and activator of transcription (STAT) signal transduction pathway in rats with collagen-induced arthritis (CIA). CIA model rats were established by the intradermal injection of bovine type II collagen emulsified in incomplete Freund’s adjuvant, followed by a booster intradermal injection. Four weeks later, the CIA model rats were treated with 42.86 μg retinol equivalents/kg body weight (b.w.) VitA or 200 mg/kg b.w. VitE for four weeks. The levels of leptin, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-10, IL-4, C-reactive protein (CRP) and rheumatic factor were measured by ELISA using commercial kits, and the erythrocyte sedimentation rate (ESR) was determined. In addition, the expression levels of phosphorylated (p)-STAT1, p-STAT3 and leptin in the synovium were evaluated by western blot analysis. The results indicated that VitA and VitE significantly reduced the levels of leptin, TNF-α, IL-6 and CRP and the ESR and significantly increased the levels of IL-10 compared with those of the model group. Furthermore, significantly reduced p-STAT3 protein expression levels were observed in the VitA and VitE groups. In conclusion, VitA and VitE reduced the levels of serum leptin protein and other cytokines. Furthermore, VitA and VitE also reduced the p-STAT3 protein levels. The present study may provide a novel approach for the treatment of RA.
机译:瘦蛋白已被确定为类风湿关节炎(RA)炎症网络中的重要细胞因子。血清瘦素水平升高可能会加速RA的发展。这项研究旨在检查维生素A(VitA)和维生素E(VitE)对瘦素水平及其他相关实验和临床指标的影响,并探讨通过Janus激酶/信号转导子和激活剂激活这些作用的机制。胶原诱导的关节炎(CIA)大鼠体内转录(STAT)信号转导途径。通过皮内注射在不完全弗氏佐剂中乳化的牛II型胶原蛋白,然后进行强化皮内注射来建立CIA模型大鼠。四周后,用42.86μg视黄醇当量/ kg体重(b.w.)VitA或200mg / kg b.w.治疗CIA模型大鼠。 VitE持续了四个星期。瘦素,肿瘤坏死因子-α(TNF-α),白介素(IL)-6,IL-10,IL-4,C反应蛋白(CRP)和风湿因子的水平使用商用试剂盒通过ELISA测定,测定红细胞沉降率(ESR)。另外,通过蛋白质印迹分析评价滑膜中磷酸化的(p)-STAT1,p-STAT3和瘦蛋白的表达水平。结果表明,与模型组相比,VitA和VitE显着降低了瘦素,TNF-α,IL-6和CRP和ESR的水平,并显着提高了IL-10的水平。此外,在VitA和VitE组中观察到p-STAT3蛋白表达水平显着降低。总之,VitA和VitE降低了血清瘦素蛋白和其他细胞因子的水平。此外,VitA和VitE还降低了p-STAT3蛋白水平。本研究可能为RA的治疗提供一种新颖的方法。

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