Eleutheroside E Ameliorates Arthritis Severity in Collagen-Induced Arthritis Mice Model by Suppressing Inflammatory Cytokine Release

被引:43
作者
He, Chunyan [1 ]
Chen, Xiaohui [1 ]
Zhao, Chunyang [2 ]
Qie, Yanyan [1 ]
Yan, Zhaowei [3 ]
Zhu, Xueming [1 ]
机构
[1] Soochow Univ, Affiliated Hosp 2, Dept Clin Lab, Suzhou, Peoples R China
[2] Soochow Univ, Affiliated Hosp 2, Dept Radiol, Suzhou, Peoples R China
[3] Soochow Univ, Affiliated Hosp 1, Dept Clin Pharmacol, Suzhou, Peoples R China
基金
中国国家自然科学基金;
关键词
eleutheroside E; rheumatoid arthritis; inflammatory cytokines; treatment; NECROSIS-FACTOR-ALPHA; RHEUMATOID-ARTHRITIS; MONOCLONAL-ANTIBODY; ACANTHOPANAX-SENTICOSUS; DOUBLE-BLIND; TNF-ALPHA; KAPPA-B; INTERLEUKIN-6; PLACEBO; INFLIXIMAB;
D O I
10.1007/s10753-014-9880-7
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Rheumatoid arthritis is the most common arthritis and is mainly characterized by symmetric polyarticular joint disorders. Eleutheroside E (EE), a principal active constituent of Acanthopanax senticosus, is reported to have anti-inflammatory effect by inhibiting NF-kappa B activities. However, the effects of EE on rheumatoid arthritis (RA) severity are largely unknown. The purpose of this study was to indicate whether EE could ameliorate arthritis and reduce inflammatory cytokine release in collagen-induced arthritis (CIA) mice. The results showed that EE attenuated the severity of arthritis by reducing the mean arthritis score and arthritis incidence. EE also significantly decreased the inflammatory cell infiltration, pannus formation, cartilage damage, and bone erosion of CIA mice. Furthermore, EE caused a marked decrease of the production of TNF-alpha and IL-6 in vivo and in vitro. These observations identify a novel function of EE that results in inhibition of cytokine release, highlighting EE was a potential therapeutic agent for RA.
引用
收藏
页码:1533 / 1543
页数:11
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