PDF(Pubmed)
Abstract：
UNASSIGNED: 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.
UNASSIGNED: 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).
UNASSIGNED: 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.
UNASSIGNED: Taken together, YSTB possesses anti-inflammatory and prevention bone destruction effects in RA disease by regulating the JAK/STAT3/SOCS3 signaling pathway.
UNASSIGNED: 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).
UNASSIGNED: 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.
UNASSIGNED: Taken together, YSTB possesses anti-inflammatory and prevention bone destruction effects in RA disease by regulating the JAK/STAT3/SOCS3 signaling pathway.
摘要：
■益肾通痹汤（YSTB），传统的中国处方，多年来一直被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作用的分子机制尚不清楚.
■这项研究的目的是研究YSTB如何影响患有胶原蛋白诱导的关节炎（CIA）的小鼠和脂多糖（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)，肿瘤坏死因子-α（TNF-α）等促炎细胞因子的表达下调，白细胞介素-1β（IL-1β），IL-6和IL-17，同时上调抗炎如IL-10和转化生长因子-β（TGF-β）的水平。同时,YSTB抑制骨侵蚀，减少炎症细胞浸润，滑膜增生,CIA小鼠的关节破坏。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）的产生和活性氧（ROS）的形成。YSTB还抑制诱导型一氧化氮合酶的产生，并减少促炎细胞因子TNF-α的释放，IL-1β,和IL-6在LPS诱导的RAW264.7细胞中的表达。此外，YSTB可以抑制JAK2、JAK3、STAT3、p38、ERK和p65蛋白的磷酸化表达,而SOCS3的表达可以被激活。
■放在一起，YSTB通过调节JAK/STAT3/SOCS3信号通路在RA疾病中具有抗炎和预防骨破坏的作用。
■这项研究的目的是研究YSTB如何影响患有胶原蛋白诱导的关节炎（CIA）的小鼠和脂多糖（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)，肿瘤坏死因子-α（TNF-α）等促炎细胞因子的表达下调，白细胞介素-1β（IL-1β），IL-6和IL-17，同时上调抗炎如IL-10和转化生长因子-β（TGF-β）的水平。同时,YSTB抑制骨侵蚀，减少炎症细胞浸润，滑膜增生,CIA小鼠的关节破坏。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）的产生和活性氧（ROS）的形成。YSTB还抑制诱导型一氧化氮合酶的产生，并减少促炎细胞因子TNF-α的释放，IL-1β,和IL-6在LPS诱导的RAW264.7细胞中的表达。此外，YSTB可以抑制JAK2、JAK3、STAT3、p38、ERK和p65蛋白的磷酸化表达,而SOCS3的表达可以被激活。
■放在一起，YSTB通过调节JAK/STAT3/SOCS3信号通路在RA疾病中具有抗炎和预防骨破坏的作用。
