Abstract

Background Traditional Chinese medicine considers that rheumatoid arthritis (RA) is caused by blood stasis, heat, and toxins. Xuebijing (XBJ), a traditional Chinese medicine compound injection, activates blood circulation to dissipate blood stasis, eliminating pathogenic heat from the blood and degrading toxins. XBJ was approved by the China FDA to treat for many years. This study examined the potential therapeutic effects of XBJ on RA and rat collagen-induced arthritis (CIA). Methods XBJ was cultured with the synovial fluid (SF) of RA patients. XBJ was also injected into CIA rats. Changes in Treg and Th17 cell levels in the peripheral blood (PB), SF, and spleen and changes in Th1/Th2 and cytokine levels in PB were detected using flow cytometry. Four RA patients were treated using XBJ based on Chinese medical theory and Chinese medicine indications. Results Following culture with XBJ, the proportion of Treg cells (P=0.007) was significantly increased in RA SF, while the Th1/Th2 ratio remained unchanged. After XBJ treatment, CIA in rats was significantly relieved (P=0.007) was significantly increased in RA SF, while the Th1/Th2 ratio remained unchanged. After XBJ treatment, CIA in rats was significantly relieved (β, IL-6, IL-17A, IFN-γ, and TNF-α decreased (P=0.007) was significantly increased in RA SF, while the Th1/Th2 ratio remained unchanged. After XBJ treatment, CIA in rats was significantly relieved (P=0.007) was significantly increased in RA SF, while the Th1/Th2 ratio remained unchanged. After XBJ treatment, CIA in rats was significantly relieved (P=0.007) was significantly increased in RA SF, while the Th1/Th2 ratio remained unchanged. After XBJ treatment, CIA in rats was significantly relieved (P=0.007) was significantly increased in RA SF, while the Th1/Th2 ratio remained unchanged. After XBJ treatment, CIA in rats was significantly relieved (P=0.007) was significantly increased in RA SF, while the Th1/Th2 ratio remained unchanged. After XBJ treatment, CIA in rats was significantly relieved (Conclusion XBJ can restore the immune balance to treat RA and CIA. Therefore, XBJ could be a potential therapeutic drug for RA.

Highlights

  • Rheumatoid arthritis (RA) is a common autoimmune disease [1, 2]

  • T regulatory (Treg) cells are differentiated from CD4+ Tcells [4]. ey can inhibit macrophage production of Tumor necrosis factor α (TNF-α) and IL-6 inflammatory cytokines, directly contact dendritic cells, and inhibit the expression of major histocompatibility complex (MHC) II molecules to reduce their antigen presentation abilities [5,6,7]. erefore, Treg cells play an antiinflammatory role in RA. e functions of T helper 17 ( 17) cells are opposite to those of Treg cells. 17 cells secrete IL17A to induce TNF-α and IL-6 expression and mediate inflammatory cell infiltration. is causes articular cartilage and bone injury, thereby playing a proinflammatory role in RA [8]. e balance between Treg cells and 17 cells has been considered an important cause of RA development [9]

  • After culturing the clinically collected synovial fluid (SF) samples from RA patients with XBJ for 48 h, the proportion of Treg cells was significantly increased (P 0.007) compared to that in the group treated with PBS as a control (Figure 1(a))

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Summary

Introduction

Rheumatoid arthritis (RA) is a common autoimmune disease [1, 2]. Tumor necrosis factor α (TNF-α) and interleukin (IL-6) levels are significantly elevated in RA, which stimulates osteoclast formation and the destruction of the articular cartilage and bone and simultaneously induces the production of other inflammatory cytokines [3].T regulatory (Treg) cells are differentiated from CD4+ Tcells [4]. ey can inhibit macrophage production of TNF-α and IL-6 inflammatory cytokines, directly contact dendritic cells, and inhibit the expression of major histocompatibility complex (MHC) II molecules to reduce their antigen presentation abilities [5,6,7]. erefore, Treg cells play an antiinflammatory role in RA. e functions of T helper 17 ( 17) cells are opposite to those of Treg cells. 17 cells secrete IL17A to induce TNF-α and IL-6 expression and mediate inflammatory cell infiltration. is causes articular cartilage and bone injury, thereby playing a proinflammatory role in RA [8]. e balance between Treg cells and 17 cells has been considered an important cause of RA development [9]. Tumor necrosis factor α (TNF-α) and interleukin (IL-6) levels are significantly elevated in RA, which stimulates osteoclast formation and the destruction of the articular cartilage and bone and simultaneously induces the production of other inflammatory cytokines [3]. Erefore, Treg cells play an antiinflammatory role in RA. Is causes articular cartilage and bone injury, thereby playing a proinflammatory role in RA [8]. E balance between Treg cells and 17 cells has been considered an important cause of RA development [9]. Traditional Chinese medicine considers that rheumatoid arthritis (RA) is caused by blood stasis, heat, and toxins. Xuebijing (XBJ), a traditional Chinese medicine compound injection, activates blood circulation to dissipate blood stasis, eliminating pathogenic heat from the blood and degrading toxins. XBJ was approved by the China FDA to treat for many years

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