左金丸对 DSS 诱导结肠炎相关的肠道微生物群和 Treg 细胞的调节作用。
Regulatory effect of Zuojin Pill on correlation with gut microbiota and Treg cells in DSS-induced colitis.
机构信息
Office of Academic Research, Jiangxi University of Traditional Chinese Medicine, Nanchang, 330004, Jiangxi Province, China.
Department of Postgraduate, Jiangxi University of Traditional Chinese Medicine, Nanchang, 330004, Jiangxi Province, China.
出版信息
J Ethnopharmacol. 2020 Nov 15;262:113211. doi: 10.1016/j.jep.2020.113211. Epub 2020 Jul 30.
ETHNOPHARMACOLOGICAL RELEVANCE
As a classic prescription and commercial Chinese patent medicine, Zuojin Pill (ZJP) has been used to treat ulcerative colitis (UC) effectively for many years. However, its mechanism of action remains unclear.
AIM OF THE STUDY
METHODS: Mice with dextran-sulfate-sodium-induced colitis were treated with ZJP for 7 d. In the present study, the therapeutic effect of ZJP was evaluated by macroscopic and microscopic observation; regulatory T (Treg) cells and their subsets were analyzed by flow cytometry; and the composition of gut microbiota was tested by 16S rRNA analysis. Activation of the phosphoinostide 3-kinase (PI3K)/Akt signaling pathway was observed by western blotting.
RESULTS
The pathological damage was attenuated and expression of proinflammatory cytokines was decreased. While the diversity of intestinal microflora was regulated, the relative abundance of Actinobacteria, and Sphingobacteriia was modified. Meanwhile, the level of CD4CD25Foxp3 and PD-L1 Treg cells improved. These changes maintained a positive correlation which was analyzed statistically. Our results also showed that ZJP inhibited activation of the PI3K/Akt signaling pathway.
CONCLUSIONS
ZJP regulates crosstalk between intestinal microflora and Treg cells to attenuate experimental colitis via the PI3K/Akt signaling pathway.
民族药理学相关性
作为经典方剂和商业中药专利，左金丸（ZJP）多年来一直被用于有效治疗溃疡性结肠炎（UC）。然而，其作用机制尚不清楚。
研究目的
方法：采用葡聚糖硫酸钠诱导的结肠炎小鼠模型，用 ZJP 治疗 7 天。在本研究中，通过宏观和微观观察评估 ZJP 的治疗效果；通过流式细胞术分析调节性 T（Treg）细胞及其亚群；通过 16S rRNA 分析测试肠道微生物组的组成。通过 Western blot 观察磷酸肌醇 3-激酶（PI3K）/Akt 信号通路的激活情况。
结果
病理损伤减轻，促炎细胞因子表达减少。在调节肠道微生物群多样性的同时，改变了放线菌和鞘脂单胞菌的相对丰度。同时，CD4+CD25+Foxp3+和 PD-L1+Treg 细胞水平提高。这些变化保持了正相关，经统计学分析。我们的结果还表明，ZJP 通过 PI3K/Akt 信号通路抑制激活。
结论
ZJP 通过 PI3K/Akt 信号通路调节肠道微生物群与 Treg 细胞之间的串扰，从而减轻实验性结肠炎。
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