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首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Kuijieling-Containing Serum Regulates Th17 and Treg Cell Differentiation by Inhibiting STAT3 Signaling In Vitro
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Kuijieling-Containing Serum Regulates Th17 and Treg Cell Differentiation by Inhibiting STAT3 Signaling In Vitro

机译:含Kuijieling的血清通过在体外抑制STAT3信号传导来调节TH17和Treg细胞分化

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Object. To investigate the effect of Kuijieling (KJL) on the balance between T helper 17 (Th17) and regulatory T (Treg) cells in peripheral blood mononuclear cells (PBMC) in vitro and explore the underlying mechanism. Materials and Methods. PBMCs isolated from rats were stimulated with transforming growth factor-β, interleukin (IL)-6, and IL-23 to induce the imbalance of Th17 and Treg cells and were treated with 10, 5, or 2.5% KJL-containing serum. The proportion of Th17 or Treg cells in CD4+ T cells was analyzed by flow cytometry, the concentrations of IL-17, IL-21, and IL-10 were assayed by ELISA, mRNA expressions of retinoic acid-related orphan receptor γt (RORγt), forkhead box protein 3 (Foxp3), and signal transducer and activator of transcription 3 (STAT3) were quantified by PCR, and phosphorylated STAT3 (p-STAT3) was analyzed by flow cytometry. Results. KJL-containing serum decreased the proportion of Th17 cells and increased the proportion of Treg cells in CD4+ T cells, decreased the concentration of IL-17 and IL-21, enhanced the level of IL-10 in the cell culture supernatant, promoted the expression of Foxp3, and inhibited the levels of RORγt, STAT3, and p-STAT3. Conclusion. KJL suppresses the STAT3 pathway to remedy the imbalance between Th17 and Treg cells.
机译:目的。探讨Kuijieling(KJL)对外周血单核细胞(PBMC)在外周血单核细胞(PBMC)中T辅助17(TH17)和调节性T(Treg)细胞之间的平衡的影响,探讨下面的机制。材料和方法。用转化生长因子-β,白细胞介素(IL)-6和IL-23刺激从大鼠分离的PBMCs促进Th17和Treg细胞的不平衡,并用10,5或2.5%的含KJL血清处理。通过流式细胞术分析CD4 + T细胞中Th17或Treg细胞的比例,ELISA测定IL-17,IL-21和IL-10的浓度,所述维甲酸相关孤儿受体γt(RORγT)的mRNA表达式通过PCR定量叉头箱蛋白3(FoxP3)和转录3(STAT3)的信号传感器和活化剂,并通过流式细胞术分析磷酸化的STAT3(P-Stat3)。结果。含KJL的血清降低了Th17细胞的比例并增加了CD4 + T细胞中的Treg细胞的比例,降低了IL-17和IL-21的浓度,增强了细胞培养上清液中IL-10的水平,促进了表达Foxp3,并抑制RORγT,STAT3和P-STAT3的水平。结论。 KJL抑制了Stat3路径以补救TH17和TREG细胞之间的不平衡。

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