Open AccessAstragaloside IV alleviates mouse slow transit constipation by modulating gut microbiota profile and promoting butyric acid generation
Author(s) -
He Qiulan,
Han Changpeng,
Huang Liang,
Yang Haojie,
Hu Jiancong,
Chen Huaxian,
Dou Ruoxu,
Ren Donglin,
Lin Hongcheng
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15586
Subject(s) - butyrate , butyric acid , gut flora , lactobacillus reuteri , loperamide , short chain fatty acid , valeric acid , chemistry , interstitial cell of cajal , lactobacillus , pharmacology , diarrhea , medicine , biology , biochemistry , immunohistochemistry , fermentation
Gut microbiota and short‐chain fatty acids (SCFAs) are associated with the development of various human diseases. In this study, we examined the role of astragaloside IV in modulating mouse gut microbiota structure and the generation of SCFAs, as well as in slow transit constipation (STC). An STC model was established by treating mice with loperamide, in which the therapeutic effects of astragaloside IV were evaluated. The microbiota community structure and SCFA content were analysed by 16S rRNA gene sequencing and gas chromatography‐mass spectrometry, respectively. The influence of butyrate on STC was assessed using a mouse model and Cajal cells (ICC). Astragaloside IV promoted defecation, improved intestinal mobility, suppressed ICC loss and alleviated colonic lesions in STC mice. Alterations in gut microbiota community structure in STC mice, such as decreased Lactobacillus reuteri diversity, were improved following astragaloside IV treatment. Moreover, astragaloside IV up‐regulated butyric acid and valeric acid, but decreased isovaleric acid, in STC mouse stools. Butyrate promoted defecation, improved intestinal mobility, and enhanced ICC proliferation by regulating the AKT–NF‐κB signalling pathway. Astragaloside IV promoted intestinal transit in STC mice and inhibited ICC loss by regulating the gut microbiota community structure and generating butyric acid.