Abstract
Jatrorrhizine hydrochloride (JH), an active component isolated from the traditional Chinese herb Coptis chinensis, has been reported to have antimicrobial, antitumor, antihypercholesterolemic, and neuroprotective activities. However, its antirheumatoid arthritis (RA) property remains unknown. In this study, a collagen-induced arthritis (CIA) rat model was used to evaluate the therapeutic effects of JH on RA by using arthritis score, radiological evaluation, and histopathological assessment. The in vitro effects of JH on proliferation, migration, and production of inflammatory mediators in RA-derived fibroblast-like synoviocyte MH7A cells were determined by the EdU incorporation assay, wound healing assay, real-time PCR, and ELISA, respectively. The in vivo studies showed that JH treatment significantly prevented the progression and development of RA in CIA rats through anti-inflammation and suppressing bone destruction. The in vitro studies revealed that JH could effectively attenuate the destructive phenotypes of MH7A cells, including inhibiting proliferation, migration, and production of inflammatory mediators. Further mechanistic analysis demonstrated that JH suppressed tumor necrosis factor alpha (TNFα)-stimulated activations of nuclear factor of kappaB (NF-κB) and mitogen-activated protein kinases (MAPKs) (ERK and p38) leading to the downregulation of proinflammatory cytokines, which might be beneficial to the antiproliferative and antimigratory activities of FLS cells. Collectively, our results demonstrated that JH has a great potential to be developed into a novel therapeutic agent for treating RA.
Highlights
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by joint inflammation and bone erosions [1]
Increasing evidence indicates that activated RA fibroblast-like synoviocytes (FLSs), which are present in great numbers in rheumatoid arthritis synovium, exhibit the characteristics of malignant cells and participate in almost all of the pathological events [5,6,7]
We demonstrated that Jatrorrhizine hydrochloride (JH) effectively attenuated the severity of RA though suppressing inflammatory responses
Summary
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by joint inflammation and bone erosions [1]. Despite the etiology and pathogenesis of RA being poorly understood, several cell types including T cells, macrophages, B cells, osteoclasts, and chondrocytes, have been demonstrated to be involved in destructive processes of the RA joint [2,3,4]. Increasing evidence indicates that activated RA fibroblast-like synoviocytes (FLSs), which are present in great numbers in rheumatoid arthritis synovium, exhibit the characteristics of malignant cells and participate in almost all of the pathological events [5,6,7]. The aggressive proliferation and migration of FLSs and their secretions such as proinflammatory cytokines and matrix-degrading enzymes lead to synovial hyperplasia, persistent synovitis, and joint damage in RA patients [6,8].
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