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王痹片通过 NF-κB 和 STAT3 信号通路对佐剂性关节炎大鼠的抑制作用。

Suppressive effects of Wang‑Bi Tablet on adjuvant‑induced arthritis in rats via NF‑κB and STAT3 signaling pathways.

机构信息

Department of Pharmacology, School of Pharmacy, Fudan University, Shanghai 201203, P.R. China.

Central Research Institute, Shanghai Pharmaceuticals Holding Co., Ltd., Shanghai 201203, P.R. China.

出版信息

Int J Mol Med. 2018 Sep;42(3):1666-1674. doi: 10.3892/ijmm.2018.3723. Epub 2018 Jun 8.

DOI:10.3892/ijmm.2018.3723
PMID:29901091
Abstract

Rheumatoid arthritis (RA) severely affects the quality life of patients due to its high association with disability. Traditional Chinese medicines have been reported to exert notable therapeutic effects on RA. The Chinese medicinal prescription Wang‑Bi Tablet (WB) has been successfully used to clinically treat RA for many years; however, its pharmacological mechanism of action is largely unclear. In the present study, adjuvant‑induced arthritis (AIA) rats were used to evaluate the anti‑inflammatory effects of WB and western blotting was used to explore the molecular mechanisms. The experimental results demonstrated that WB treatment significantly reduced arthritis score and hind‑paw volume. Furthermore, synovial hyperplasia, inflammatory cell infiltration and joint destruction were ameliorated by WB. The expression levels of the proinflammatory cytokines interleukin (IL)‑1β, tumor necrosis factor‑α and IL‑6, were reduced in the joints of WB‑treated rats. Western blotting revealed that WB could also inhibit excessive activation of nuclear factor (NF)‑κB and Janus kinase (JAK)‑signal transducer and activator of transcription 3 (STAT3) signaling pathways. These results indicated that the therapeutic effects of WB on AIA may be accomplished through inhibition of the NF‑κB and JAK‑STAT3 signaling pathways. These findings provide experimental evidence to support WB as a therapeutic agent for the treatment of patients with RA.

摘要

类风湿性关节炎(RA)由于其与残疾高度相关,严重影响患者的生活质量。据报道,中药对 RA 具有显著的治疗作用。中药方剂完带汤(WB)已成功用于临床治疗 RA 多年,但其药理作用机制尚不清楚。本研究采用佐剂诱导关节炎(AIA)大鼠模型评价 WB 的抗炎作用,并采用 Western blot 探讨其分子机制。实验结果表明,WB 治疗可显著降低关节炎评分和后爪体积。此外,WB 还可改善滑膜增生、炎性细胞浸润和关节破坏。WB 治疗可降低关节中促炎细胞因子白细胞介素(IL)-1β、肿瘤坏死因子-α和 IL-6 的表达水平。Western blot 结果显示,WB 还可抑制核因子(NF)-κB 和 Janus 激酶(JAK)-信号转导和转录激活因子 3(STAT3)信号通路的过度激活。这些结果表明,WB 治疗 AIA 的疗效可能是通过抑制 NF-κB 和 JAK-STAT3 信号通路实现的。这些发现为 WB 作为治疗 RA 患者的治疗药物提供了实验依据。

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