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首页> 外文期刊>Cytokine >Majoon ushba, a polyherbal compound ameliorates rheumatoid arthritis via regulating inflammatory and bone remodeling markers in rats
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Majoon ushba, a polyherbal compound ameliorates rheumatoid arthritis via regulating inflammatory and bone remodeling markers in rats

机译：Majoon ushba，一种多草药化合物，通过调节大鼠的炎症和骨重塑标志物来改善类风湿关节炎

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The present study was aimed to investigate the anti-arthritic effect of majoon ushba (MU) and its underlying mechanism in adjuvant induced arthritis (AIA) rats. Arthritis was induced by intradermal injection of complete freund's adjuvant (0.1 ml) into the right hind paw of the Wistar albino rats. MU (1000 mg/kg/b. wt) and methotrexate (3 mg/kg/b. wt) were administered from day 11 to day 18th for 8 days after adjuvant induction. We have found that MU treatment significantly increased the level of anti-inflammatory cytokine (IL-10) and inhibited the over production of pro-inflammatory cytokines (TNF-alpha, IL-1 beta, and IL-6) and monocyte chemoattractant protein-1 (MCP-1) (ELISA) in the serum of adjuvant-induced arthritic rats. The mRNA expression of pro-inflammatory cytokines (TNF-alpha, IL-1 beta, IL-6, and IL-17), inflammatory enzymes (inducible nitric oxide synthase (iNOS) and cyclo-oxygenase-2 (COX-2)), MCP-1, receptor activator of nuclear factor-kB ligand (RANKL) and transcription factors (NF-kappa B and AP-1) (Real-Time PCR) was found significantly downregulated in the synovial tissues of MU treated arthritic rats. In addition, the protein expression of NF-kappa B, IL-17, COX-2, and RANKL (western blotting and immunohistochemistry analysis) was found reduced. On the other hand, osteoprotegerin (OPG), a bone remodeling marker was found to be elevated in synovial tissues of MU treated arthritic rats. Furthermore, MU treatment prevented body weight loss and reduced the joint paw edema, cell infiltration, cartilage and bone degradation as evidenced by the histopathological and radiological analysis. In conclusion, our current findings provide scientific evidence for the traditional claim of MU as an anti-arthritic drug. (C) 2015 Elsevier Ltd. All rights reserved.
机译：本研究的目的是研究佐剂（Majoon ushba）（MU）的抗关节炎作用及其在佐剂性关节炎（AIA）大鼠中的潜在机制。通过将完全弗氏佐剂（0.1 ml）皮内注射到Wistar albino大鼠的右后爪中诱发关节炎。在佐剂诱导后第11天至第18天施用MU（1000mg / kg / b.wt）和甲氨蝶呤（3mg / kg / b.wt）8天。我们发现MU治疗可显着提高抗炎细胞因子（IL-10）的水平，并抑制促炎性细胞因子（TNF-alpha，IL-1 beta和IL-6）和单核细胞趋化蛋白-佐剂诱导的关节炎大鼠血清中的1（MCP-1）（ELISA）。促炎细胞因子（TNF-α，IL-1 beta，IL-6和IL-17），炎性酶（诱导型一氧化氮合酶（iNOS）和环加氧酶-2（COX-2））的mRNA表达。在MU处理过的关节炎大鼠的滑膜组织中，MCP-1，核因子-kB配体的受体激活剂（RANKL）和转录因子（NF-κB和AP-1）（实时PCR）被显着下调。另外，发现NF-κB，IL-17，COX-2和RANKL的蛋白质表达降低（Western印迹和免疫组织化学分析）。另一方面，骨重塑标志物骨保护蛋白（OPG）在MU治疗的关节炎大鼠的滑膜组织中被发现升高。此外，MU的治疗可以防止体重减轻，并减轻关节爪水肿，细胞浸润，软骨和骨降解，如组织病理学和放射学分析所证明的那样。总之，我们目前的发现为MU作为抗关节炎药的传统主张提供了科学依据。 （C）2015 Elsevier Ltd.保留所有权利。

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