Inhibitory effects of tubeimoside I on synoviocytes and collagen-induced arthritis in rats

被引:18
作者
Liu, Zhenzhou [1 ,2 ]
Zhou, Lin [3 ]
Ma, Xuemei [1 ,2 ]
Sun, Shengnan [1 ,2 ]
Qiu, Haiwen [1 ,2 ]
Li, Hui [1 ,2 ]
Xu, Jiake [3 ]
Liu, Mei [1 ,2 ]
机构
[1] Nanjing Normal Univ, Jiangsu Key Lab Mol & Med Biotechnol, Nanjing 210023, Jiangsu, Peoples R China
[2] Nanjing Normal Univ, Coll Life Sci, Nanjing 210023, Jiangsu, Peoples R China
[3] Univ Western Australia, Sch Biomed Sci, Perth, WA, Australia
基金
英国医学研究理事会; 中国国家自然科学基金;
关键词
collagen-induced arthritis; fibroblast-like synoviocytes; rheumatoid arthritis; tubeimoside I; FIBROBLAST-LIKE SYNOVIOCYTES; NF-KAPPA-B; RHEUMATOID-ARTHRITIS; SYNOVIAL-FLUID; GROWTH-FACTOR; PHASE ARREST; GELATINASE B; FACTOR-BETA; CELLS; PATHWAY;
D O I
10.1002/jcp.26754
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Advancements in rheumatoid arthritis (RA) therapies have shown considerable progresses in the comprehension of disease. However, the development of new potential medicines with relative safety and efficacy continues and natural compounds have been considered as alternatives or complementary agents to gain immense attractions. Tubeimoside I (TBMS I), a main triterpenoid saponin isolated from Bolbostemma paniculatum, has been reported to possess antiviral and anticancer effects. However, its effect on RA remains unknown. Here, we investigated the therapeutic effect of TBMS I in collagen-induced arthritis (CIA) rats and explored its underlying mechanism. Our results showed that TBMS I treatment efficaciously ameliorated inflammation and joint destruction of rats with CIA. In vitro studies revealed that TBMS I suppressed the production of pro-inflammatory cytokines including IL-1, IL-6, IL-8 and TNF, and downregulated the expression of MMP-9. In addition, TBMS I attenuated the destructive phenotypes of FLS of CIA rats including inhibiting proliferation and reducing migration rate. Further mechanistic analysis demonstrated that TBMS I suppressed TNF-induced activations of NF-B and MAPKs (p38 and JNK) leading to the downregulation of pro-inflammatory cytokines, which was beneficial to the anti-proliferative and anti-migratory activities of FLS cells. Taken together, TBMS I has a great potential to be developed into a novel therapeutic agent for the treatment of RA.
引用
收藏
页码:8740 / 8753
页数:14
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