Dextran-Sulfate-Sodium-Induced Colitis-Ameliorating Effect of Aqueous Phyllanthus emblica L. Extract through Regulating Colonic Cell Gene Expression and Gut Microbiomes.
Xiaoqing LiWen OuyangYiqi JiangQianru LinXinan PengHao HuZhuming YeGuo LiuYong CaoYigang YuPublished in: Journal of agricultural and food chemistry (2023)
The anti-inflammation effect of aqueous Phyllanthus emblica L. extract (APE) and its possible underlying mechanism in dextran sulfate sodium (DSS)-induced mice chronic colonic inflammation were studied. APE treatment significantly improved the colitic symptoms, including ameliorating the shortening of the colon, increasing the DSS-induced body weight loss, reducing the disease activity index, and reversing the condition of colon tissue damage of mucus lost and goblet cell reduction. Overproduction of serum pro-inflammatory cytokines were suppressed by the treatment of APE. Gut microbiome analysis showed that APE remodeled the structure of gut bacteria in phylum and genus levels, upregulating the abundance of phylum Bacteroidetes, family Muribaculaceae, and genus Bacteroides and downregulating the abundance of phylum Firmicutes. The reshaped gut microbiome caused metabolic functions and pathway change with enhanced queuosine biosynthesis and reduced polyamine synthesis pathway. Colon tissue transcriptome analysis further elucidated APE-inhibited mitogen-activated protein kinase (MAPK), cytokine-cytokine receptor interaction, and tumor necrosis factor (TNF) signaling pathways and the expressions of the genes that promote the progress of colorectal cancer. It turned out that APE reshaped the gut microbiome and inhibited MAPK, cytokine-cytokine receptor interaction, and TNF signaling pathways as well as the colorectal-cancer-related genes to exert its colitis protective effect.
Keyphrases
- oxidative stress
- rheumatoid arthritis
- signaling pathway
- disease activity
- diabetic rats
- gene expression
- pi k akt
- single cell
- weight loss
- high glucose
- drug induced
- ulcerative colitis
- systemic lupus erythematosus
- anti inflammatory
- cell therapy
- mesenchymal stem cells
- rheumatoid arthritis patients
- microbial community
- ankylosing spondylitis
- dna methylation
- bone marrow
- stem cells
- depressive symptoms
- combination therapy
- epithelial mesenchymal transition
- transcription factor
- juvenile idiopathic arthritis
- antibiotic resistance genes
- cell proliferation
- bariatric surgery
- insulin resistance