Abstract
Paeoniflorin-6′-O-benzene sulfonate (code: CP-25) was the chemistry structural modifications of Paeoniflorin (Pae). CP-25 inhibited B cells proliferation stimulated by B cell activating factor belonging to the TNF family (BAFF) or Tumor necrosis factor alpha (TNF-alpha). CP-25, Rituximab and Etanercept reduced the percentage and numbers of CD19+ B cells, CD19+CD20+ B cells, CD19+CD27+ B cells and CD19+CD20+CD27+ B cells induced by BAFF or TNF-alpha. There was significant difference between CP-25 and Rituximab or CP-25 and Etanercept. CP-25 down-regulated the high expression of BAFFR, BCMA, and TACI stimulated by BAFF or TNF-alpha. The effects of Rituximab and Etanercept on BAFFR or BCMA were stronger than that of CP-25. CP-25, Rituximab and Etanercept down-regulated significantly the expression of TNFR1 and TNFR2 on B cell stimulated by BAFF or TNF-alpha. CP-25, Rituximab and Etanercept down-regulated the expression of MKK3, P-p38, P-p65, TRAF2, and p52 in B cells stimulated by BAFF and the expression of TRAF2 and P-p65 in B cells stimulated by TNF-alpha. These results suggest that CP-25 regulated moderately activated B cells function by regulating the classical and alternative NF-κB signaling pathway mediated by BAFF and TNF-alpha-TRAF2-NF-κB signaling pathway. This study suggests that CP-25 may be a promising anti-inflammatory immune and soft regulation drug.
Highlights
B cells derive from bone marrow pluripotent stem cells and account for 15% of peripheral blood leukocytes (Tobon et al, 2013)
The Effects of CP-25 on the Percentage and Numbers of B Cell Subsets Stimulated by BAFF and TNF-alpha
These results suggest that CP-25 regulates B cells function and inhibits the maturation of B cells induced by BAFF through the classical and alternative NF-κB signaling pathway mediated by BAFF
Summary
B cells derive from bone marrow pluripotent stem cells and account for 15% of peripheral blood leukocytes (Tobon et al, 2013). B cells have lots of key roles, including presenting antigen, secreting pro-inflammatory cytokines and antibodies, and activating T cells (Namm et al, 2012; Bugatti et al, 2014). The efficacy of B cell depletion therapy shows that B cells play a critical role in the pathogenesis of autoimmune diseases (Leandro, 2009). B cell subsets can be distinguished corresponding to different stages of differentiation, maturation and activation, which are characterized by the expression of different surface markers, such as CD19, CD20, and CD27 (Maecker et al, 2012; Leandro, 2013). CD27 is a key marker of memory B cells and can promote memory B cells to differentiate into plasma cells (Han et al, 2016)
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