Treatment with Recombinant Hsp72 Suppresses Collagen-Induced Arthritis in Mice

被引:17
作者
Luo, Xinjing [1 ,2 ]
Zuo, Xiaoxia [3 ]
Mo, Xuanrong [2 ]
Zhou, Yaou [3 ]
Xiao, Xianzhong [1 ]
机构
[1] Cent S Univ, Xiangya Sch Med, Dept Pathophysiol, Changsha 410078, Hunan, Peoples R China
[2] Taizhou Univ, Coll Med, Inst Cell Biol, Taizhou 318000, Zhejiang, Peoples R China
[3] Cent S Univ, Xiangya Hosp, Dept Rheumatol & Clin Immunol, Changsha 410008, Hunan, Peoples R China
基金
中国国家自然科学基金;
关键词
arthritis; animal models; heat shock protein; cytokines; signal pathways; NF-KAPPA-B; HEAT-SHOCK PROTEINS; NECROSIS-FACTOR-ALPHA; RHEUMATOID-ARTHRITIS; INFLAMMATORY ARTHRITIS; SYNOVIAL FIBROBLASTS; MONOCLONAL-ANTIBODY; CYTOKINE PRODUCTION; ADJUVANT ARTHRITIS; P65; SUBUNIT;
D O I
10.1007/s10753-010-9250-z
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Although the level of heat shock protein (Hsp72) has been shown to be enhanced in rheumatoid arthritis (RA) synovial tissues and RA synovial fluid, it remains unclear what role extracellular Hsp72 plays in the pathogenesis of RA. This study was conducted to investigate the effects of recombinant human Hsp72 on collagen-induced arthritis (CIA) when administered therapeutically and elucidate its underlying mechanism. We demonstrated that recombinant Hsp72 significantly reduced disease severity. Hsp72-treated animals displayed significantly less cartilage and bone destruction than that in the controls. Hsp72 treatment also reduced the expression of tumor necrosis factor alpha and interleukin 6 in the sera. Furthermore, Hsp72 treatment significantly inhibited activation of nuclear factor kappa B (NF-kappa B) in synovial tissues of CIA mice. These findings suggest that recombinant Hsp72 effectively suppressed synovial inflammation and the development and progress of CIA, which is mediated through the reduction of production of proinflammatory cytokines and the suppression of activation of NF-kappa B pathway.
引用
收藏
页码:432 / 439
页数:8
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