Fig 1.
Effects of trilobatin (TLB)on the pathological symptoms of mice with dextran sodium sulfate (DSS)-induced ulcerative colitis (UC).
(A) Structural formula of TLB. (B) Schematic representation of the experimental design. (C) Body weight (g) measured daily. (D) Disease activity index (DAI) score. (E) Representative images of colon and colon length. Data are expressed as mean ± standard deviation (SD). ** P < 0.05 vs. control (n = 7).
Table 1.
Primers and their sequences used for qRT-PCR.
Fig 2.
Effects of TLB on colonic inflammation and mucosal barrier damage in mice DSS-induced UC.
(A) Representative images of hematoxylin-eosin (HE)-stained colon tissue sections (scale bar = 50 μm; magnification, × 200). (B) Expression levels of three inflammatory cytokines (TNF-α, IL-1β, and IL-6) in the sera of mice measured by ELISA. (C) Expression levels of genes encoding three inflammatory cytokines (TNF-α, IL-1β, and IL-6) in colon tissue measured by quantitative real-time PCR (qRT-PCR. (D) Expression of mRNA levels of genes encoding tight junction proteins (ZO-1 and occludin) in colon tissue measured by qRT-PCR. (E) Protein levels of tight junction proteins (ZO-1 and occludin) in colon tissue measured by western blotting analysis. Data are expressed as mean ± SD. ** P < 0.05 vs. control (n = 7).
Fig 3.
NF-κB pathway was inhibited by TLB in mice with DSS-induced UC.
(A) Levels of the NF-κB pathway-associated proteins (p-p65, t-p65, p-IKB-α, and t-IKB-α) detected by western blotting analysis. (B) Levels of the PI3K/Akt pathway-associated proteins (p-Akt and t-Akt) detected by western blotting analysis. Data are expressed as mean ± SD. ** P < 0.05 vs. control. “ns” indicates no significant difference.
Fig 4.
Composition of gut microbiota modulated by TLB in mice with DSS-induced UC.
(A) Venn diagram showing the bacterial taxa in three groups of mice. (B) Average relative abundance of the top 10 taxa at the phylum or class levels. (C) Heatmap of microbial relative abundance and taxa clustering. (D) Phylogenetic tree of gut microbiota at the genus level. (E) Ternary plot of the top 10 microbial taxa.
Fig 5.
Relative abundance and diversity of gut microbiota modulated by TLB in mice with DSS-induced UC.
(A) Species accumulation boxplot. (B) α diversity analysis based on the Chao1, observed_OTUs, Shannon, and pielou_e indices. (C) Distance matrix heatmap. (D) Hierarchical cluster tree based on the relative abundance of the top 10 bacterial phyla. (E) Bray–Curtis-based principal component analysis (PCA) and principal coordinate analysis (PCoA) plots based on unweighted UniFrac.
Fig 6.
Specific differential bacterial taxa of gut microbiota modulated by TLB in mice with DSS-induced UC.
(A) Taxonomic cladogram. (B) Linear discriminant analysis effect size (LEfSe) analysis of gut microbiota among the three groups of mice with linear discriminant analysis (LDA) score > 4.
Fig 7.
Functional prediction of gut microbiota modulation by TLB in mice with DSS-induced UC.
(A) Relative abundance of function prediction annotation represented in the column. (B) Relative abundance of function prediction annotation represented in cluster heatmap. (C) Functional differences between groups based on t-test (P < 0.05).
Fig 8.
Schematic illustration of the main findings reported in this study.
TLB alleviates the pathological symptoms, inflammation, and colonic mucosal barrier damage in mice with DSS-induced UC via the inhibition of the NF-κB pathway and alteration of gut microbiota composition (created with BioRender.com).