Ginsenoside Rg1 relieves experimental colitis by regulating balanced differentiation of Tfh/Treg cells
Ginsenoside Rg1 relieves experimental colitis by regulating balanced differentiation of Tfh/Treg cells
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人参皂苷 Rg1 通过调节 Tfh/Treg 细胞平衡分化缓解实验性结肠炎
DOI：
10.1016/j.intimp.2021.108133
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发表时间：
2021-09-20
影响因子：
5.6
通讯作者：
Liu, Duanyong
中科院分区：
文献类型：
--
作者：
Jin, Jing;Zhong, Youbao;Liu, Duanyong
炎症性肠病（IBD）的典型特征在于Tfh细胞分化的失调。我们试图通过观察结肠炎小鼠Tfh/Treg细胞水平和PI 3 K/Akt信号通路的激活来探讨人参皂甙Rg 1（G-Rg 1）治疗IBD的潜在机制。在本研究中，G-Rg 1显著抑制葡聚糖硫酸钠（DSS）诱导的小鼠结肠炎的炎症反应，表现为体重和结肠长度增加，结肠重量减少，结肠重量指数和组织病理学评分降低，IL-6和TNF-α水平降低，IL-10水平升高。显著地，G-Rg 1有效地降低了CD 4（+）CXCR 5（+）IL-9（+）（Tfh 9）、CD 4（+）CXCR 5（+）IL-17（+）（Tfh 17）的量，并增加了CD 4（+）CXCR 5（+）Foxp 3（+）（Tfr）和CD 4（+）CD 25（+）Foxp 3（+）（Treg）细胞。此外，G-Rg 1还能显著下调PI 3 K和p-Akt的表达，上调PTEN的表达。提示G-Rg 1能有效调节Tfh/Treg细胞平衡，减轻实验性结肠炎，其机制可能与抑制PI 3 K/Akt信号通路有关。
Inflammatory bowel disease (IBD) is typically characterized by the dysregulation of Tfh cell differentiation. we sought to explore the potential mechanism of Ginsenoside Rg1 (G-Rg1) treated IBD by observing the level of the Tfh/Treg cells and the activation of PI3K/Akt signaling pathway in the colitis mice. In the present study, G-Rg1 significantly inhibited the inflammatory response to mice colitis induced by dextran sodium sulfate (DSS), as evidenced by increased body weight and colon length, decreased colon weight, reduced colon weight index and histopathological scores, lower levels of IL-6 and TNF-alpha, and increased IL-10 levels. Significantly, G-Rg1 effectively decreased the amounts of CD4(+)CXCR5(+)IL-9(+)(Tfh9), CD4(+) CXCR5(+)IL-17(+)(Tfh17), and increased CD4(+)CXCR5(+)Foxp3(+)(Tfr) and CD4(+)CD25(+) Foxp3(+)(Treg) cells. Furthermore, G-Rg1 markedly down-regulated PI3K and p-Akt level, and upregulated PTEN expression. These results indicated that G-Rg1 could effectively regulate the balance of Tfh/Treg cells to relieve experimental colitis, which could be potentially related to PI3K/Akt signaling pathway inhibition.