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Ginsenoside Rg1 relieves experimental colitis by regulating balanced differentiation of Tfh/Treg cells
International Immunopharmacology ( IF 5.6 ) Pub Date : 2021-09-20 , DOI: 10.1016/j.intimp.2021.108133
Jing Jin 1 , Youbao Zhong 1 , Jian Long 1 , Tiantian Wu 1 , Qingqing Jiang 1 , Haiyan Wang 2 , Wei Ge 3 , Haimei Zhao 4 , Duanyong Liu 5
Affiliation  

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-α, 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.



中文翻译:

人参皂甙 Rg1 通过调节 Tfh/Treg 细胞的平衡分化缓解实验性结肠炎

炎症性肠病 (IBD) 的典型特征是 Tfh 细胞分化失调。我们试图通过观察结肠炎小鼠中 Tfh/Treg 细胞的水平和 PI3K/Akt 信号通路的激活来探索人参皂甙 Rg1 (G-Rg1) 治疗 IBD 的潜在机制。在本研究中,G-Rg1 显着抑制葡聚糖硫酸钠 (DSS) 诱导的小鼠结肠炎炎症反应,表现为体重和结肠长度增加、结肠重量降低、结肠重量指数和组织病理学评分降低、 IL-6 和 TNF-α,并增加 IL-10 水平。显着的是,G-Rg1 有效降低了 CD4 + CXCR5 + IL-9 + (Tfh9)、CD4 + CXCR5的数量+ IL-17 + (Tfh17),并增加 CD4 + CXCR5 + Foxp3 + (Tfr) 和 CD4 + CD25 + Foxp3 + (Treg) 细胞。此外,G-Rg1 显着下调 PI3K 和 p-Akt 水平,上调 PTEN 表达。这些结果表明G-Rg1可以有效调节Tfh/Treg细胞平衡以缓解实验性结肠炎,这可能与抑制PI3K/Akt信号通路有关。

更新日期:2021-09-20
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