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盐酸青藤碱对类风湿关节炎患者外周血单个核细胞增殖、细胞因子产生及调节性 T 细胞频率的影响。

Effects of sinomenine on the proliferation, cytokine production, and regulatory T-cell frequency in peripheral blood mononuclear cells of rheumatoid arthritis patients.

机构信息

Department of Pharmacy, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, China.

Institute of Traditional Chinese Medicine, Hubei Province Academy of Traditional Chinese Medicine, Wuhan, China.

出版信息

Drug Dev Res. 2021 Apr;82(2):251-258. doi: 10.1002/ddr.21748. Epub 2020 Oct 2.

DOI:10.1002/ddr.21748
PMID:33006164
Abstract

Sinomenine (SN) is a plant-derived alkaloid isolated from Caulis Sinomenii. It has been approved by the State Food and Drug Administration of China for treating rheumatoid arthritis (RA) nearly 20 years ago. To investigate the anti-RA mechanism of SN, a lot of scholars reported the immunosuppressive effect of SN on T lymphocytes. We continued to evaluate the suppressive function of SN by using human peripheral blood mononuclear cells (PBMCs) isolated from RA patients. As the positive control, 10 ng/ml of methylprednisolone (MP) showed the antiproliferation effect on mitogen-activated PBMCs of RA patients significantly (*p < .05). Meanwhile, MP decreased the frequency of CD4 CD25 T cells and suppressed the secretion of inflammatory Th1/Th2/Th17 cytokines such as IL-4, IL-6, IL-10, IL-17, IFN-γ, and TNF-α. However, SN at concentrations of 0.3-30 μM, showed little suppressive effects on the proliferation of PBMCs of RA patients. We did not observe any suppressive effects of SN on percentages of CD4 T cells and CD4 CD25 T cells in the mitogen-activated PBMCs of RA patients. The influence of SN on the percentage of CD4 CD25 Foxp3 T cells was also limited. Finally, even 30 μM of SN did not influence the secretion of Th1/Th2/Th17 cytokine significantly. The present study provided evidence that anti-RA mechanism of SN seems not to be related with the suppressive effects on peripheral T cells.

摘要

青藤碱(SN)是从青风藤中提取的一种植物源性生物碱。近 20 年前,它已被中国国家食品药品监督管理局批准用于治疗类风湿关节炎(RA)。为了研究 SN 的抗 RA 机制,许多学者报道了 SN 对 T 淋巴细胞的免疫抑制作用。我们继续使用从 RA 患者中分离的人外周血单核细胞(PBMC)来评估 SN 的抑制功能。作为阳性对照,10ng/ml 的甲泼尼龙(MP)对 RA 患者有丝分裂原激活的 PBMC 的增殖有明显的抑制作用(*p<0.05)。同时,MP 降低了 CD4 CD25 T 细胞的频率,并抑制了炎症性 Th1/Th2/Th17 细胞因子如 IL-4、IL-6、IL-10、IL-17、IFN-γ和 TNF-α的分泌。然而,SN 在 0.3-30μM 的浓度下,对 RA 患者 PBMC 的增殖几乎没有抑制作用。我们没有观察到 SN 对 RA 患者有丝分裂原激活的 PBMC 中 CD4 T 细胞和 CD4 CD25 T 细胞的比例有任何抑制作用。SN 对 CD4 CD25 Foxp3 T 细胞比例的影响也有限。最后,即使 30μM 的 SN 也没有明显影响 Th1/Th2/Th17 细胞因子的分泌。本研究提供的证据表明,SN 的抗 RA 机制似乎与对外周 T 细胞的抑制作用无关。

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