Zhuang Yuanyuan, Liu Jiabao, Ma Pei, Bai Jinye, Ding Yasi, Yang Hui, Fan Yannan, Lin Mingbao, Li Shuai, Hou Qi
State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing, China.
Front Pharmacol. 2017 Aug 15;8:538. doi: 10.3389/fphar.2017.00538. eCollection 2017.
Tamarixinin A, a natural tannin isolated from , has been confirmed to have moderate anti-inflammatory effects and . However, how it effects rheumatoid arthritis (RA) is still unknown. Therefore, the aim of this study is to investigate the therapeutic effects of tamarixinin A on experimental RA, and explore the underlying mechanism. The anti-arthritic effects of tamarixinin A were evaluated on collagen-induced arthritis (CIA) mice and adjuvant-induced arthritis (AIA) rats. The hind paw thickness, inflammatory cytokine levels in serum, and histopathological assessments were determined. The arthritis score was evaluated. Activation of p38 and p65 in AIA rats was also determined. The anti-inflammatory effect was also tested in LPS induced macrophages, and its related anti-inflammatory signaling pathways were explored. Treatment with tamarixinin A significantly suppressed the progression and development of RA in CIA mice and AIA rats. Both in CIA mice and AIA rats, arthritis scores decreased, paw swelling and thickness were reduced, and joint destruction was alleviated. In AIA rats, tamarixinin A significantly inhibited the expression of p38, p-p38 and p65. In addition, tamarixinin A inhibited the production of pro-inflammatory mediators, the phosphorylation of p38, ERK, JNK and p65, as well as the nuclear translocation of p38 in LPS- induced macrophages. Tamarixinin A is a potential effective candidate compound for human RA treatment, which executes anti-arthritic effects potentially through down-regulating MAPK and NF-κB signal pathway activation.
没食子酸A是从[具体来源未给出]中分离出的一种天然单宁，已被证实具有中等程度的抗炎作用[此处原文似乎不完整]。然而，其对类风湿性关节炎（RA）的影响仍不清楚。因此，本研究的目的是探讨没食子酸A对实验性RA的治疗作用，并探索其潜在机制。在胶原诱导的关节炎（CIA）小鼠和佐剂诱导的关节炎（AIA）大鼠上评估了没食子酸A的抗关节炎作用。测定了后爪厚度、血清中炎性细胞因子水平和组织病理学评估结果。评估了关节炎评分。还测定了AIA大鼠中p38和p65的激活情况。在脂多糖诱导的巨噬细胞中测试了其抗炎作用，并探索了其相关的抗炎信号通路。没食子酸A治疗显著抑制了CIA小鼠和AIA大鼠中RA的进展和发展。在CIA小鼠和AIA大鼠中，关节炎评分均降低，爪肿胀和厚度减小，关节破坏得到缓解。在AIA大鼠中，没食子酸A显著抑制p38、p-p38和p65的表达。此外，没食子酸A抑制促炎介质的产生、p38、ERK、JNK和p65的磷酸化，以及脂多糖诱导的巨噬细胞中p38的核转位。没食子酸A是治疗人类RA的一种潜在有效候选化合物，其可能通过下调MAPK和NF-κB信号通路激活来发挥抗关节炎作用。
