Rheumatoid arthritis (RA) is a common autoimmune disease which impacts a large number of patients worldwide, and new drugs are required for lower the disease burden. Theaflavin-3, 3'-digallate (TFDG) is polyphenol exhibiting inhibition on inflammatory factors. This study aimed to explore the attenuation of TFDG on RA. The collagen-induced arthritis (CIA) mouse model was established and administered with TFDG. The arthritis score and incidence was recorded to assess the amelioration of TFDG on arthritis. Histopathological change of the mouse joint tissues was evaluated by haemotoxylin and eosin staining. The expression of pro-inflammatory mediators including interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and IL-6 was quantified by ELISA. The activation of nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) signaling pathways in the synovium were determined by Western blotting. In comparison with the control, administration of TFDG significantly reduced arthritis score and incidence in the CIA mouse model. TFDG significantly suppressed the expression of IL-1β, TNF-α, and IL-6, as well as the levels of MMP-1, MMP-2, and MMP-3 in the synovium. TFDG also showed remarkable inhibition on the activation of NF-κB and the phosphorylation of P38, JNK2, and ERK. This study puts up evidence that TFDG exerts protection on RA via inhibiting the activation of NF-κB- and MAPK-signaling pathways.

中文翻译：

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Theaflavin-3，3'-Digallate通过核因子-κB和MAPK途径减轻小鼠的类风湿炎症。

类风湿关节炎（RA）是一种常见的自身免疫性疾病，会影响全世界的大量患者，因此需要新药来降低疾病负担。Theaflavin-3，3'-digallate（TFDG）是对炎症因子具有抑制作用的多酚。本研究旨在探讨TFDG对RA的衰减作用。建立胶原诱导的关节炎（CIA）小鼠模型，并与TFDG一起给药。记录关节炎评分和发病率以评估TFDG对关节炎的改善。通过苏木精和曙红染色评估小鼠关节组织的组织病理学变化。通过ELISA定量测定促炎介质包括白介素（IL）-1β，肿瘤坏死因子（TNF）-α和IL-6的表达。通过蛋白质印迹法确定滑膜中核因子（NF）-κB和丝裂原激活的蛋白激酶（MAPK）信号通路的激活。与对照组相比，在CIA小鼠模型中，TFDG的给药显着降低了关节炎评分和发病率。TFDG显着抑制滑膜中IL-1β，TNF-α和IL-6的表达以及MMP-1，MMP-2和MMP-3的水平。TFDG还显示出对NF-κB的活化和P38，JNK2和ERK磷酸化的显着抑制作用。这项研究提供了证据，表明TFDG通过抑制NF-κB-和MAPK信号通路的激活对RA起到保护作用。TFDG显着抑制滑膜中IL-1β，TNF-α和IL-6的表达以及MMP-1，MMP-2和MMP-3的水平。TFDG还显示出对NF-κB的活化和P38，JNK2和ERK磷酸化的显着抑制作用。这项研究提供了证据，表明TFDG通过抑制NF-κB-和MAPK信号通路的激活对RA发挥保护作用。TFDG显着抑制滑膜中IL-1β，TNF-α和IL-6的表达以及MMP-1，MMP-2和MMP-3的水平。TFDG还显示出对NF-κB活化和P38，JNK2和ERK磷酸化的显着抑制作用。这项研究提供了证据，表明TFDG通过抑制NF-κB和MAPK信号通路的激活对RA起到保护作用。