miR-155/GSK-3β 通过抑制 LPS 诱导的 RAW264.7 细胞中的 NF-κB 信号通路介导柴胡皂苷 IVa 的抗炎作用。

MiR-155/GSK-3β mediates anti-inflammatory effect of Chikusetsusaponin IVa by inhibiting NF-κB signaling pathway in LPS-induced RAW264.7 cell.

机构信息

Affiliated Renhe Hospital of China Three Gorges University, Yichang, 443001, Hubei, China.

College of Medical Science, China Three Gorges University, Yichang, 443002, Hubei, China.

出版信息

Sci Rep. 2020 Oct 27;10(1):18303. doi: 10.1038/s41598-020-75358-1.

It has been demonstrated that Chikusetsusaponin IVa (CsIVa) possesses abundant biological activities. Herein, using LPS to establish acute inflammation model of mouse liver and cell line inflammation model, we investigated whether miR-155/GSK-3β regulated NF-κB signaling pathway, and CsIVa exerted anti-inflammatory effects by regulating miR-155/GSK-3β signaling pathway. Our results showed that LPS induced high expression of miR-155 and miR-155 promoted macrophage activation through GSK-3β. In addition, CsIVa inhibited inflammatory responses in LPS-induced mouse liver and RAW264.7 cells. Furthermore, we demonstrated that CsIVa improved the inflammatory response in LPS-induced RAW264.7 cells by inhibiting miR-155, increasing GSK-3β expression, and inhibiting NF-κB signaling pathway. In conclusion, our study reveals that CsIVa suppresses LPS-triggered immune response by miR-155/GSK-3β-NF-κB signaling pathway.

已经证明，柴胡皂苷 IVa（CsIVa）具有丰富的生物活性。在此，我们使用 LPS 建立了小鼠肝急性炎症模型和细胞系炎症模型，研究了 miR-155/GSK-3β 是否调节 NF-κB 信号通路，以及 CsIVa 是否通过调节 miR-155/GSK-3β 信号通路发挥抗炎作用。我们的结果表明，LPS 诱导 miR-155 的高表达，并且 miR-155 通过 GSK-3β 促进巨噬细胞的激活。此外，CsIVa 抑制 LPS 诱导的小鼠肝和 RAW264.7 细胞中的炎症反应。此外，我们证明 CsIVa 通过抑制 miR-155、增加 GSK-3β 表达和抑制 NF-κB 信号通路来改善 LPS 诱导的 RAW264.7 细胞中的炎症反应。总之，我们的研究表明 CsIVa 通过 miR-155/GSK-3β-NF-κB 信号通路抑制 LPS 触发的免疫反应。