Fuzi lizhong pills alter microbial community compositions and metabolite profiles in ulcerative colitis rat with spleen-kidney yang deficiency syndrome

溃疡性结肠炎 代谢物 脾脏 医学 药丸 传统医学 生理学 药理学 内科学 疾病
作者
Yin-lin Zhou,Jing Wu,Hongliang Wang,Wuwen Feng,Peng Fu,Ruoqi Zhang,Hong-Ling Yan,Juan Liu,Yuzhu Tan,Cheng Peng
出处
期刊:Journal of Ethnopharmacology [Elsevier]
卷期号:335: 118645-118645 被引量:1
标识
DOI:10.1016/j.jep.2024.118645
摘要

Ulcerative colitis (UC) is a chronic inflammatory bowel condition that is frequently related with Spleen-Kidney Yang Deficiency Syndrome (SKYD) in Chinese medicine. Fuzi Lizhong Pill (FLZP), a traditional medicine for SKYD, has been utilized in China for generations, although the exact mechanism by which it treats UC is unknown. The goal of this study is to further understand FLZP's therapeutic mechanism in SKYD-associated UC. To investigate the impact of FLZP on SKYD-associated UC, we used a comprehensive method that included serum metabolomics and gut microbiota profiling. The chemical composition of FLZP was determined using mass spectrometry. UC rats with SKYD were induced and treated with FLZP. Serum metabolomics and 16S rRNA microbial community analysis were used to evaluate FLZP's effects on endogenous metabolites and gut microbiota, respectively. Correlation analysis investigated the association between metabolites and intestinal flora. A metabolic pathway analysis was undertaken to discover putative FLZP action mechanisms. FLZP contains 109 components, including liquiritin (584.8176 μg/g), benzoylaconine (16.3087 μg/g), benzoylhypaconine (31.9583), and hypaconitine (8.1160 μg/g). FLZP predominantly regulated seven metabolites and eight metabolic pathways involved in amino acid and nucleotide metabolism, with an emphasis on energy metabolism and gastrointestinal digestion. FLZP also influenced intestinal flora variety, increasing probiotic abundance while decreasing pathogenic bacteria prevalence. An integrated investigation identified associations between changes in certain gut flora and energy metabolism, specifically the tricarboxylic acid (TCA) cycle. FLZP successfully cures UC in SKYD rats by regulating amino acid and energy metabolism. Its positive effects may include altering microbiota composition and metabolite profiles in UC rats with SKYD. These findings shed light on FLZP's mode of action and its implications for UC management. • FLZP primarily regulates metabolic pathways related to amino acid and nucleotide metabolism. • FLZP may treat UC rats in SKYD by modulating the species richness and diversity of intestinal flora. • Some gut bacteria changes in UC rats with SKYD link to TCA cycle energy metabolism. • FLZP's relief of UC in SKYD rats may involve microbiota and metabolite changes.
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