College of Medicine and Institute of Biomedical Science and Technology, Konkuk University, Chungju, Korea.
J Pharm Pharmacol. 2012 Mar;64(3):420-9. doi: 10.1111/j.2042-7158.2011.01415.x. Epub 2011 Dec 8.
We aimed to determine the anti-arthritis effect and its mechanism of a combination of herbal extracts from Trachelospermi caulis (TC) and Moutan cortex radicis (MC) (TCMC).
The anti-arthritis activity of TCMC was assessed using a mouse model of type II collagen-induced arthritis (CIA). Reverse transcriptase-polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), electrophoretic mobility shift assay (EMSA) and other biological assays were performed.
TCMC significantly ameliorated various inflammatory parameters, such as clinical arthritis index, histological deformation of joints, serum levels of rheumatoid arthritis biomarkers (cartilage oligomeric matrix protein, serum amyloid P and anti-collagen type II IgG antibody), and Th1-related responses (T cell proliferation, and production of Interferon-γ and interleukin (IL)-2 in splenocytes isolated from CIA mice). The production of matrix metalloproteinases (MMPs), pro-inflammatory cytokines (tumour necrosis factor-α, IL-1β and IL-6) and chemokines (macrophage inflammatory protein-1, monocyte chemoattractant protein-1, and Regulated upon Activation, Normal T-cell Expressed, and Secreted) was suppressed by TCMC in CIA mice. In addition, the number of osteoclasts in the hind tibia was significantly decreased. With regard to the mechanism, TCMC suppressed the activation of the transcription factors nuclear factor (NF)-κB and activator protein (AP)-1.
TCMC exerts an anti-arthritis effect in CIA mice by suppression of the production of various inflammatory factors and the formation of osteoclasts through the inhibition of NF-κB and AP-1 activation.
本研究旨在探讨藤仲(TC)和牡丹皮(MC)草药提取物组合(TCMC)的抗关节炎作用及其机制。
采用Ⅱ型胶原蛋白诱导的关节炎(CIA)小鼠模型评估 TCMC 的抗关节炎活性。进行逆转录聚合酶链反应(RT-PCR)、酶联免疫吸附测定(ELISA)、电泳迁移率变动分析(EMSA)等生物检测。
TCMC 显著改善了各种炎症参数,如临床关节炎指数、关节组织学变形、类风湿关节炎生物标志物(软骨寡聚基质蛋白、血清淀粉样蛋白 P 和抗胶原类型 II IgG 抗体)、Th1 相关反应(T 细胞增殖和 CIA 小鼠脾细胞产生干扰素-γ和白细胞介素(IL)-2)。TCMC 抑制 CIA 小鼠基质金属蛋白酶(MMPs)、促炎细胞因子(肿瘤坏死因子-α、IL-1β 和 IL-6)和趋化因子(巨噬细胞炎症蛋白-1、单核细胞趋化蛋白-1 和活化正常 T 细胞表达和分泌)的产生。此外,后肢胫骨破骨细胞数量明显减少。在机制上,TCMC 通过抑制核因子(NF)-κB 和激活蛋白(AP)-1 的激活来抑制各种炎症因子的产生和破骨细胞的形成,从而发挥抗关节炎作用。
TCMC 通过抑制 NF-κB 和 AP-1 的激活,抑制各种炎症因子的产生和破骨细胞的形成,从而发挥抗 CIA 小鼠关节炎的作用。