ABSTRACT
Sweet tea (Lithocarpus litseifolius [Hance] Chun) is a new resource for food raw materials, with plenty of health functions. This study aimed to investigate the preventive effect and potential mechanism of sweet tea extract (STE) against ulcerative colitis (UC). Briefly, BABL/c mice were treated with STE (100 and 400 mg/kg) for 2 weeks to prevent 3% dextran sulfate sodium (DSS)-induced UC. It was found that STE supplementation significantly prevented DSS-induced UC symptoms; suppressed the levels of pro-inflammatory mediators, such as myeloperoxidase and tumor necrosis factor-α; increased the levels of anti-inflammatory cytokines; and up-regulated the expression of tight junction proteins (Zonula occludens-1 and Occludin). STE also altered the gut microbiota profile of UC mice by increasing Bacteroidetes, Lactobacillus, Akkermansia, Lachnospiraceae_NK4A136_group, and Alistipes and inhibiting Firmicutes, Proteobacteria, and Helicobacter, accompanied by a significant increase in the content of butyric acid. Moreover, STE increased the expression of G-protein-coupled receptor (GPR) 43 and GPR109A and inhibited the expression of histone deacetylase 3 (HDAC3) and nuclear factor-κB p65 (NF-κB p65) in the colon. In conclusion, this study indicated that STE has a good preventive effect on UC by regulating gut microbiota to activate butyrate-GPR-mediated anti-inflammatory signaling and simultaneously inhibit HDAC3/NF-κB inflammatory signaling.
Subject(s)
Colitis, Ulcerative , Colitis , Gastrointestinal Microbiome , Animals , Anti-Inflammatory Agents/therapeutic use , Butyric Acid/metabolism , Colitis/chemically induced , Colitis/metabolism , Colitis/prevention & control , Colitis, Ulcerative/chemically induced , Colitis, Ulcerative/drug therapy , Colitis, Ulcerative/prevention & control , Colon/metabolism , Dextran Sulfate/adverse effects , Disease Models, Animal , Mice , Mice, Inbred C57BL , NF-kappa B/metabolism , Tea/adverse effectsABSTRACT
Changes in gene expression occur as animals, including primates, age. Macaques have long been used as a model species for primate evolution and biomedical studies. Here, to study gene expression in Tibetan macaques (Macaca thibetana, TMs) and its differences to humans, we applied RNA-Seq to obtain the blood transcriptomes of 24 TMs. In total, 2 523 age-associated differentially expressed genes (DEGs) were identified. Several pathways and processes that regulate aging, including the FoxO signaling pathway, autophagy, and platelet activation, were significantly enriched in the up-regulated DEGs. Two significantly age-related modules were identified by weighted gene co-expression network analysis (WGCNA). The TMs and humans shared 279 common DEGs, including 111 up-regulated and 141 down-regulated genes with advancing age in the same expression direction. However, 27 age-related DEGs presented the opposite expression direction in TMs as that in humans. For example, INPPL1, with inhibitory effects on the B cell receptor signaling pathway, was up-regulated in humans but down-regulated in TMs. In general, our study suggests that aging is a critical factor affecting gene expression in the captive TM population. The similarities and differences in gene expression patterns between TMs and humans could provide new insights into primate evolution and benefit TM model development.
