Department of Medical Immunology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Rev Physiol Biochem Pharmacol. 2021;179:1-29. doi: 10.1007/112_2020_54.
Rheumatoid arthritis (RA) is a chronic immune-mediated inflammatory disorder characterized by the destruction of the joint and bone resorption. The production of pro-inflammatory cytokines and chemokines, dysregulated functions of three important subtypes of T helper (T) cells including T1, T17, and regulator T (Treg) cells are major causes of the initiation and development of RA. Moreover, B cells as a source of the production of several autoantibodies play key roles in the pathogenesis of RA. The last decades have seen increasingly rapid advances in the field of immunopharmacology using natural origin compounds for the management of various inflammatory diseases. Curcumin, a main active polyphenol compound isolated from turmeric, curcuma longa, possesses a wide range of pharmacologic properties for the treatment of several diseases. This review comprehensively will assess beneficial immunomodulatory effects of curcumin on the production of pro-inflammatory cytokines and also dysregulated functions of immune cells including T1, T17, Treg, and B cells in RA. We also seek the clinical efficacy of curcumin for the treatment of RA in several recent clinical trials. In conclusion, curcumin has been found to ameliorate RA complications through modulating inflammatory and autoreactive responses in immune cells and synovial fibroblast cells via inhibiting the expression or function of pro-inflammatory mediators, such as nuclear factor-κB (NF-κB), activated protein-1 (AP-1), and mitogen-activated protein kinases (MAPKs). Of note, curcumin treatment without any adverse effects can attenuate the clinical symptoms of RA patients and, therefore, has therapeutic potential for the treatment of the diseases.
类风湿关节炎（RA）是一种慢性免疫介导的炎症性疾病，其特征是关节破坏和骨质吸收。促炎细胞因子和趋化因子的产生、三种重要的辅助性 T 细胞亚群（T1、T17 和调节性 T（Treg）细胞）功能失调是 RA 起始和发展的主要原因。此外，B 细胞作为产生几种自身抗体的来源，在 RA 的发病机制中发挥关键作用。在过去的几十年中，利用天然来源的化合物在管理各种炎症性疾病方面，免疫药理学领域取得了越来越快的进展。姜黄素是从姜黄中分离出来的主要活性多酚化合物，具有广泛的药理特性，可用于治疗多种疾病。本综述全面评估了姜黄素对促炎细胞因子产生和 RA 中免疫细胞（包括 T1、T17、Treg 和 B 细胞）功能失调的有益免疫调节作用。我们还研究了姜黄素在几项最近的临床试验中治疗 RA 的临床疗效。总之，姜黄素通过抑制核因子-κB（NF-κB）、激活蛋白-1（AP-1）和丝裂原活化蛋白激酶（MAPKs）等促炎介质的表达或功能，调节免疫细胞和滑膜成纤维细胞中的炎症和自身反应性应答，从而改善 RA 并发症。值得注意的是，姜黄素治疗没有任何不良反应，可以减轻 RA 患者的临床症状，因此具有治疗该疾病的潜力。
