Liang Xiu-Jun, Guo Ya-Chun, Sun Tong-You, Song Hong-Ru, Gao Ya-Xian
Basic Medical Institute, Chengde Medical University, Chengde, Hebei 067000, P.R. China.
Department of Pathogen Biology, Chengde Medical University, Chengde, Hebei 067000, P.R. China.
Exp Ther Med. 2016 Oct;12(4):2155-2160. doi: 10.3892/etm.2016.3586. Epub 2016 Aug 10.
Rheumatoid arthritis (RA) is a common chronic autoimmune and incurable disease. The aim of the present study was to investigate the therapeutic effect and mechanism of the total saponins of Rhizoma (TSRDN) in RA. A collagen induced-arthritis (CIA) rat model was established. CIA rats were randomly divided into three groups and lavaged with an equal volume of solvent (CIA group), TSRDN (25 mg/kg/day, RDN group) and tripterygium (TP; 12 mg/kg/day, TP group) for 21 days, respectively. Normal rats served as a control group. Hematoxylin-eosin (HE) staining was used to observe the histopathological injury of synovial tissues. The level of CD31, which used for marking and counting, micro vessel density (MVD) and the expression levels of vascular endothelial growth factor (VEGF) and signal transducer and activator of transcription 3 (STAT3) were detected by immunohistochemical analysis. Additionally, the DNA-binding activity of nuclear factor-κB (NF-κB) was determined using an ELISA kit. HE staining showed obvious synovial hyperplasia, inflammatory cell infiltration, pannus formation, cartilage and bone erosion in the CIA group rats. In addition, compared with control group, the level of MVD, the expression of VEGF and STAT3, and the DNA-binding activity of NF-κB were all increased in CIA group rat synovial tissue (all P<0.01); however, TSRDN or tripterygium were able to inhibit these changes (all P<0.01). It was speculated that TSRDN may prevent angiogenesis by inhibiting the expression of STAT3 and the DNA-binding activity of NF-κB p65, thereby potentially improving CIA.
类风湿性关节炎(RA)是一种常见的慢性自身免疫性疾病,无法治愈。本研究旨在探讨Rhizoma总皂苷(TSRDN)对RA的治疗作用及机制。建立胶原诱导性关节炎(CIA)大鼠模型。将CIA大鼠随机分为三组,分别用等体积的溶剂(CIA组)、TSRDN(25mg/kg/天,RDN组)和雷公藤(TP;12mg/kg/天,TP组)灌胃21天。正常大鼠作为对照组。采用苏木精-伊红(HE)染色观察滑膜组织的组织病理学损伤。通过免疫组化分析检测用于标记和计数的CD31水平、微血管密度(MVD)以及血管内皮生长因子(VEGF)和信号转导子和转录激活子3(STAT3)的表达水平。此外,使用ELISA试剂盒测定核因子-κB(NF-κB)的DNA结合活性。HE染色显示CIA组大鼠滑膜明显增生、炎性细胞浸润、血管翳形成、软骨和骨侵蚀。此外,与对照组相比,CIA组大鼠滑膜组织中MVD水平、VEGF和STAT3的表达以及NF-κB的DNA结合活性均升高(均P<0.01);然而,TSRDN或雷公藤能够抑制这些变化(均P<0.01)。推测TSRDN可能通过抑制STAT3的表达和NF-κB p65的DNA结合活性来预防血管生成,从而可能改善CIA。