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Curcumin suppresses colorectal tumorigenesis through restoring the gut microbiota and metabolites
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Journal Article
Curcumin suppresses colorectal tumorigenesis through restoring the gut microbiota and metabolites
2024
Overview
Background
Curcumin has been reported to have activity for prevention and therapy of CRC, yet its underlying mechanisms remain largely unknown. Recently, emerging evidence suggests that the gut microbiota and its metabolites contribute to the causation and progression of Colorectal cancer (CRC). In this study, we aimed to investigate if curcumin affects the tumorigenesis of CRC by modulating gut microbiota and its metabolites.
Methods
Forty male C57BL/6JGpt mice were randomly divided into four groups: negative control (NC), curcumin control, CRC model, and curcumin treatment (CRC-Cur) groups. CRC mouse model was induced by using azoxymethane (AOM) and dextran sodium sulfate (DSS), and the mice in CRC model and curcumin treatment groups received oral PBS or curcumin (150 mg/kg/day), respectively. Additionally, fecal samples were collected. 16 S rRNA sequencing and Liquid Chromatography Mass Spectrometry (LC-MS)-based untargeted metabolomics were used to observe the changes of intestinal flora and intestinal metabolites.
Results
Curcumin treatment restored colon length and structural morphology, and significantly inhibited tumor formation in AOM/DSS-induced CRC model mice. The 16S rRNA sequencing analysis indicated that the diversity and richness of core and total species of intestinal microflora in the CRC group were significantly lower than those in the NC group, which were substantially restored in the curcumin treatment group. Curcumin reduced harmful bacteria, including
Ileibacterium
,
Monoglobus
and
Desulfovibrio
, which were elevated in CRC model mice. Moreover, curcumin increased the abundance of
Clostridia_UCG-014
,
Bifidobacterium
and
Lactobacillus
, which were decreased in CRC model mice. In addition, 13 different metabolites were identified. Compared to the NC group, ethosuximide, xanthosine, and 17-beta-estradiol 3-sulfate-17-(beta-D-glucuronide) were elevated in the CRC model group, whereas curcumin treatment significantly reduced their levels. Conversely, glutamylleucine, gamma-Glutamylleucine, liquiritin, ubenimex, 5’-deoxy-5’-fluorouridine, 7,8-Dihydropteroic acid, neobyakangelicol, libenzapril, xenognosin A, and 7,4’-dihydroxy-8-methylflavan were decreased in the CRC group but notably upregulated by curcumin. Kyoto Encyclopedia of Genes and Genome (KEGG) pathway analysis revealed enrichment in seven pathways, including folate biosynthesis (
P
< 0.05).
Conclusions
The gut microecological balance was disrupted in AOM/DSS-induced CRC mice, accompanied by metabolite dysbiosis. Curcumin restored the equilibrium of the microbiota and regulated metabolites, highly indicating that curcumin may alleviate the development of AOM/DSS induced colorectal cancer in mice by regulating intestinal flora homeostasis and intestinal metabolites.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,BMC
Subject
/ Animals
/ Biomedical and Life Sciences
/ Carcinogenesis - drug effects
/ Colon
/ Colorectal Neoplasms - chemically induced
/ Colorectal Neoplasms - drug therapy
/ Colorectal Neoplasms - metabolism
/ Colorectal Neoplasms - microbiology
/ Colorectal Neoplasms - pathology
/ Curcumin
/ Dextran
/ Feces
/ Gastrointestinal Microbiome - drug effects
/ Health Promotion and Disease Prevention
/ Humans
/ Male
/ Mice
/ Microbiota (Symbiotic organisms)
/ Oncology
/ RNA, Ribosomal, 16S - genetics
/ rRNA 16S
/ Taxonomy
/ Tumors
/ Turmeric
