益肾通痹汤（YSTB）是一种中药方剂，多年来一直用于改善类风湿性关节炎（RA）的症状。先前的研究表明，YSTB 具有抗炎和镇痛特性。然而，YSTB抗RA作用的潜在分子机制仍不清楚。本研究的目的是研究YSTB如何影响胶原诱导性关节炎（CIA）小鼠和脂多糖（LPS）诱导的RAW264.7细胞。研究结果表明，YSTB 可以显着改善 CIA 小鼠的临床关节炎症状（减轻爪肿胀、关节炎评分、胸腺和脾脏指数、增加体重），下调促炎细胞因子如肿瘤坏死因子-α (TNF-α) 的表达、白细胞介素-1β (IL-1β)、IL-6 和 IL-17，同时上调 IL-10 和转化生长因子-β (TGF-β) 等抗炎物质的水平。同时，YSTB 可以抑制 CIA 小鼠的骨侵蚀并减少炎症细胞浸润、滑膜增殖和关节破坏。此外，我们发现 YSTB 能够抑制 LPS 诱导的 RAW264.7 细胞炎症，这归因于抑制一氧化氮 (NO) 产生和活性氧物种 (ROS) 形成。 YSTB 还抑制 LPS 诱导的 RAW264.7 细胞中诱导型一氧化氮合酶的产生，并减少促炎细胞因子 TNF-α、IL-1β 和 IL-6 的释放。此外，YSTB还可以抑制JAK2、JAK3、STAT3、p38、ERK和p65蛋白的磷酸化表达，而激活SOCS3的表达。综上所述，YSTB在RA疾病中具有抗炎和预防骨质破坏的作用。调节 JAK/STAT3/SOCS3 信号通路。版权所有 © 2024 Xu、Jiao、Wu、Yu、Liu、Zhang 和 Chen。

Yishen-Tongbi Decoction (YSTB), a traditional Chinese prescription, has been used to improve syndromes of rheumatoid arthritis (RA) for many years. Previous research has shown that YSTB has anti-inflammatory and analgesic properties. However, the underlying molecular mechanism of the anti-RA effects of YSTB remains unclear.The purpose of this research was to investigate how YSTB affected mice with collagen-induced arthritis (CIA) and RAW264.7 cells induced with lipopolysaccharide (LPS).The findings show that YSTB could significantly improve the clinical arthritic symptoms of CIA mice (mitigate paw swelling, arthritis score, thymus and spleen indices, augment body weight), downregulated expression of pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), IL-6 and IL-17, while upregulated the level of anti-inflammatory like IL-10 and transforming growth factor-β (TGF-β). Meanwhile, YSTB inhibits bone erosion and reduces inflammatory cell infiltration, synovial proliferation, and joint destruction in CIA mice. In addition, we found that YSTB was able to suppress the LPS-induced inflammation of RAW264.7 cells, which was ascribed to the suppression of nitric oxide (NO) production and reactive oxygen species formation (ROS). YSTB also inhibited the production of inducible nitric oxide synthase and reduced the releases of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 in LPS-induced RAW264.7 cells. Furthermore, the phosphorylation expression of JAK2, JAK3, STAT3, p38, ERK and p65 protein could be suppressed by YSTB, while the expression of SOCS3 could be activated.Taken together, YSTB possesses anti-inflammatory and prevention bone destruction effects in RA disease by regulating the JAK/STAT3/SOCS3 signaling pathway.Copyright © 2024 Xu, Jiao, Wu, Yu, Liu, Zhang and Chen.