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Abstract
In traditional Chinese medicine (TCM), xianfanghuomingyin (XFHM) is used to treat autoimmune diseases, including rheumatoid arthritis (RA). Here, we studied the mechanisms underlying its treatment effects, especially its anti-inflammatory effects in a collagen-induced arthritis (CIA) mouse model. We found that cartilage destruction and pannus formation were alleviated by treatment with XFHM. The abnormal differentiation of Th1 and Th17 cells was downregulated significantly by XFHM, and Th2 and Treg cells were upregulated. Moreover, the expression levels of specific cytokines and transcription factors related to Th1 cells (interferon γ [IFNγ], T-bet) and Th17 cells (interleukin- [IL-] 17) and the nuclear receptor retinoic acid receptor-related orphan receptor-gamma (RORγ) were downregulated. Serum IL-4 and GATA-3, which contribute to Th2 cells differentiation, increased significantly after XFHM administration. These results indicate that XFHM can restore the balance of T lymphocytes and reestablish the immunological tolerance to inhibit autoinflammatory disorder of RA. Taken together, XFHM can be used as a complementary or alternative traditional medicine to treat RA.
Highlights
Rheumatoid arthritis (RA), characterized by inflammation of synovial joints, is a chronic and systemic autoimmune disease, which leads to a progressive destruction of articular cartilage and periarticular structures [1, 2]
We focused on the Chinese traditional therapy XFHM and its mechanisms of action in improving pathophysiologic characteristics of RA in Collageninduced arthritis (CIA) mice
The experimental evidences indicate that these constituents, including wanillic acid [29], loganic acid [30], paeoniflorin [31], loganin [32], apiin [33], gentiopicroside [34], astragaloside IV [35], acteoside [36], prime-Oglucosylcimifugin [37], and isoimperatorin [38], had antiinflammatory and immune-regulatory effects that inhibited the activation of NF-κB or other signaling pathways
Summary
Rheumatoid arthritis (RA), characterized by inflammation of synovial joints, is a chronic and systemic autoimmune disease, which leads to a progressive destruction of articular cartilage and periarticular structures [1, 2]. Various inflammatory cells, including T and B cells, macrophages, dendritic cells and natural killer cells, infiltrate RA joints and induce the proliferation of cells of the synovial lining [3, 4] These cells constitute the synovial lining, participate in inflammation, contribute to synovial proliferation, pannus formation and cartilage destruction and subchondral bone erosion [5]. Loss of the suppression effect of Treg cells on effector T cells can lead to loss of control of the autoimmune inflammation in RA and subsequent
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