Paeoniflorin selectively inhibits LPS-provoked B-cell function
Paeoniflorin selectively inhibits LPS-provoked B-cell function
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DOI：
10.1016/j.jphs.2015.02.011
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发表时间：
2015-05-01
影响因子：
3.5
通讯作者：
Li, Ningli
中科院分区：
文献类型：
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作者：
Zhang, Jie;Li, Huidan;Li, Ningli
B细胞在自身免疫性疾病的发生发展中起重要作用，其机制涉及异常的多克隆B细胞激活、致病抗体的产生和靶向，这些机制有效地减少了炎症和组织损伤，但往往会导致患者遭受继发感染。芍药苷(PF)是牡丹总苷的主要成分，多年来被广泛用于治疗自身免疫性疾病。然而，PF是否影响B细胞活性仍不清楚。在本研究中，我们利用纯化的小鼠脾B细胞，在体外分析了PF对B细胞功能的影响。我们发现PF能抑制CD69/CD86的表达和抑制脂多糖刺激的B细胞的增殖。此外，PF还可减少脂多糖刺激的B细胞分化和免疫球蛋白的产生。有趣的是，PF并不改变抗CD40或IL-4引起的B细胞的激活和增殖。这些结果首次表明，PF通过选择性阻断LPS/TLR4信号通路，抑制B细胞的活化、增殖和分化。此外，我们的数据表明，在自身免疫性疾病的治疗中，PF选择性地抑制由内毒素激活的B细胞介导的炎症和组织损伤，但不改变CD40/CD40L或IL-4诱导的B细胞功能，这可能有助于保护患者免受继发感染。(C)2015年提交人。由爱思唯尔B.V.代表日本药理学会制作和主办。
B cells are important in the development of autoimmune disorders through mechanisms involving dysregulated polyclonal B-cell activation, production of pathogenic antibodies, and targeting which reduces inflammation and tissue damage effectively but often leads to patients suffering from secondary infection. Paeoniflorin (PF) is the main substance of the Total glucosides of peony and has been widely used to treat autoimmune diseases for years. However, whether PF affects B cell activity remains unknown. In this study, using purified murine spleen B cells, we analyzed the effects of PF on B-cell function in vitro. We found that PF inhibited the expression of CD69/CD86 and the proliferation of B cells stimulated by LPS. In addition, PF reduced the B-cell differentiation and immunoglobulin production that was stimulated by LPS. Interestingly, PF did not alter B-cell activation and proliferation provoked by anti-CD40 or IL-4. These results indicated for the first time that PF inhibits B-cell activation, proliferation and differentiation by selectively blocking the LPS/TLR4 signaling pathway. Furthermore, our data suggest that PF selectively inhibits inflammation and tissue damage mediated by LPS-activated B cells but does not alter CD40/CD40L-or IL-4-provoked B-cell function in autoimmune diseases treatment, which might aid in protecting patients from secondary infection. (C) 2015 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society.