Rheumatoid arthritis is primarily associated with inflammation and increased level of proinflammatory cytokines which are released by immune cells, macrophages or activation of arachidonic acid metabolism. The expression of these cytokines, oxidative free radicals and the activation of COX-2 enzymes are crucial targets for chronic inflammation. On the basis of established anti-inflammatory efficacy of nerolidol, the primary study was further appraised to determine its approach against Freund’s complete adjuvant (CFA) rheumatoid model. Arthritis was induced by inoculation of 0.1 mL CFA injection into the left hind footpad of rats. Anti-arthritic potential of nerolidol (at 200, 400 and 800 mg/kg doses) was assessed by measuring the paw volume, body weight, serum analysis, histopathological and radiographs of ankle joints. Expressions of cytokine’s panels such as IL-10, IL-4, COX-2, NF-kB, TNF-α, IL-6, PGE-2 and IL-1β were determined by real-time qPCR. Antioxidant enzyme analyses were conducted by measuring the SOD, POD and catalase activity from serum and equated with arthritic control group. Nerolidol prevented body weight loss, stabilized biochemical and haematological homeostasis and significantly reduced the paw volume. Furthermore, X-ray and histopathological assessment of ankle joints showed an improvement in the joint structure of rats treated with nerolidol. Besides that, overexpression of gene pointers like TNF-α, IL-1β, IL-6, NF-kB, PGE-2 and COX-2 in CFA-treated control rats were also reversed with nerolidol. This anti-arthritic mechanism was further supported by the increased level of IL-10, IL-4 and serum antioxidant activity. The present findings demonstrate that nerolidol reduced adjuvant arthritis by downregulating the proinflammatory cytokines and upregulating the aforementioned anti-inflammatory cytokines and may be used as a therapeutic substance for the management of human rheumatoid arthritis.

类风湿性关节炎主要与炎症和免疫细胞、巨噬细胞释放的促炎细胞因子水平升高或花生四烯酸代谢激活有关。这些细胞因子的表达、氧化自由基和 COX-2 酶的激活是慢性炎症的关键靶点。在确定橙花醇的抗炎功效的基础上，进一步评估了初步研究以确定其对抗弗氏完全佐剂 (CFA) 类风湿模型的方法。通过将0.1mL CFA注射剂接种到大鼠的左后足垫中来诱发关节炎。通过测量爪体积、体重、血清分析、组织病理学和踝关节的射线照片来评估橙花醇的抗关节炎潜力（在 200、400 和 800 mg/kg 剂量下）。通过实时 qPCR 测定细胞因子组的表达，例如 IL-10、IL-4、COX-2、NF-kB、TNF-α、IL-6、PGE-2 和 IL-1β。通过测量血清中的SOD、POD和过氧化氢酶活性进行抗氧化酶分析，并等同于关节炎对照组。橙花醇可防止体重减轻，稳定生化和血液稳态，并显着减少爪子体积。此外，踝关节的 X 射线和组织病理学评估显示，用橙花醇治疗的大鼠的关节结构有所改善。除此之外，橙花醇也可以逆转 CFA 处理的对照大鼠中 TNF-α、IL-1β、IL-6、NF-kB、PGE-2 和 COX-2 等基因指针的过表达。这种抗关节炎机制得到了 IL-10、IL-4 和血清抗氧化活性水平升高的进一步支持。