4.6 Article

Yifei Sanjie Formula Treats Chronic Obstructive Pulmonary Disease by Remodeling Pulmonary Microbiota

期刊

FRONTIERS IN MEDICINE
卷 9, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fmed.2022.927607

关键词

chronic obstructive pulmonary disease; pulmonary microbiota; inflammation; Yifei Sanjie Formula; NLRP3/caspase-1L/IL-1 beta signaling pathway

资金

  1. National Natural Science Foundation of China [81860646, 81760819]
  2. Yunnan Provincial Science and Technology Department [202201AS070084, 202005AC160058, 202101AZ070001-012, 202005AF150063, 202102AE090031]
  3. Science Research Foundation of Yunnan Provincial Department of Education [2020Y0204]
  4. Yunnan Science and Technology Planning Project-Joint Major Project of Traditional Chinese Medicine [2019FF002[-002]]
  5. Provincial Innovation Team of the Yunnan University of Chinese Medicine for Traditional Chinese Medicine [2018HC011]

向作者/读者索取更多资源

In this study, the Yifei Sanjie Formula was found to have therapeutic effects on COPD by remodeling lung microbes and inhibiting inflammation signal pathways. This intervention may serve as a potential therapeutic strategy for COPD by positively influencing beneficial lung bacteria and negatively affecting pathogenic bacteria.
Chronic obstructive pulmonary disease (COPD) is one of the most common pulmonary diseases. Evidence suggests that dysbiosis of pulmonary microbiota leads to the COPD pathological process. Yifei Sanjie Formula (YS) is widely used to treat diseases in respiratory systems, yet little is known about its mechanisms. In the present study, we first established the fingerprint of YS as the background for UHPLC-QTOF-MS. Components were detected, including alkaloids, amino acid derivatives, phenylpropanoids, flavonoids, terpenoids, organic acids, phenols, and the like. The therapeutic effect of YS on COPD was evaluated, and the pulmonary function and ventilatory dysfunction (EF50, TV, and MV) were improved after the administration of YS. Further, the influx of lymphocytes was inhibited in pulmonary parenchyma, accompanied by down-regulation of inflammation cytokines via the NLRP3/caspase-1/IL-1 beta signaling pathway. The severity of pulmonary pathological damage was reversed. Disturbed pulmonary microbiota was discovered to involve an increased relative abundance of Ralstonia and Mycoplasma and a decreased relative abundance of Lactobacillus and Bacteroides in COPD animals. However, the subversive effect was shown. The abundance and diversity of pulmonary microflora were remodeled, especially increasing beneficial genua Lactobacillus and Bacteroides, as well as downregulating pathogenic genua Ralstonia and Mycoplasma in the YS group. Environmental factor correlation analysis showed that growing pulmonary microbiota was positively correlated with the inflammatory factor, referring to Ralstonia and Mycoplasma, as well as negatively correlated with the inflammatory factor, referring to Lactobacillus and Bacteroides. These results suggest that the effects of YS involved remodeling lung microbes and anti-inflammatory signal pathways, revealing that intervention microbiota and an anti-inflammatory may be a potential therapeutic strategy for COPD.

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