Ameliorating Effects of Vitamin K2 on Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice

Abstract

Ulcerative colitis (UC) is a chronic recurrent inflammatory illness of the gastrointestinal system. The purpose of this study was to explore the alleviating effect of vitamin K2 (VK2) on UC, as well as its mechanism. C57BL/6J mice were given 3% DSS for seven days to establish UC, and they then received VK2 (15, 30, or 60 mg/kg·bw) and 5-aminosalicylic acid (100 mg/kg·bw) for two weeks. We recorded the clinical signs, body weights, colon lengths, and histological changes during the experiment. We detected the inflammatory factor expressions using enzyme-linked immunosorbent assay (ELISA) kits, and we detected the tight junction proteins using Western blotting. We analyzed the intestinal microbiota alterations and short-chain fatty acids (SCFAs) using 16S rRNA sequencing and targeted metabolomics. According to the results, VK2 restored the colon lengths, improved the colonic histopathology, reduced the levels of proinflammatory cytokines (such as IL-1β, TNF-α, and IL-6), and boosted the level of the immunosuppressive cytokine IL-10 in the colon tissues of the colitis mice. Moreover, VK2 promoted the expression of mucin and tight junction proteins (such as occludin and zonula occludens-1) in order to preserve the intestinal mucosal barrier function and prevent UC in mice. Additionally, after the VK2 intervention, the SCFAs and SCFA-producing genera, such as Eubacterium_ruminantium_group and Faecalibaculum, were elevated in the colon. In conclusion, VK2 alleviated the DSS-induced colitis in the mice, perhaps by boosting the dominant intestinal microflora, such as Faecalibaculum, by reducing intestinal microflora dysbiosis, and by modulating the expression of SCFAs, inflammatory factors, and intestinal barrier proteins.

Causal effects of gut microbiota in the development of lung cancer and its histological subtypes: A Mendelian randomization study

“…In an animal experiment, the usage of vitamin K2 in mice with colitis led to an increase in the abundance of Eubacterium ruminantium group in the colon, thereby alleviating colitis. 39 An MR analysis demonstrated that Eubacterium ruminantium group was negatively correlated with bone mineral density. 40 Moreover, our study revealed that this GM taxon was a protective factor for SCLC.…”

Faecalibacterium prausnitzii prevents hepatic damage in a mouse model of NASH induced by a high-fructose high-fat diet

“…The abundance of Lachnospiraceae_NK4A136_group was significantly higher in the EB-FPDK11-treated group than in the NASH group ( Supplementary Figure S3E ), and this genus has been reported to play a role in maintaining the integrity of the intestinal barrier ( Ma et al, 2020 ). In addition to Lachnospiraceae_NK4A136_group , Gemella , the proportion of which was increased in the EB-FPDK11-treated group, has reported to be positively correlated with the expression of tight junction proteins ( Hu et al, 2023 ). The altered microbiota in the F. prausnitzii -treated group may have influenced the strength of the gut barrier, indicating a potential connection between the two.…”

Anti-Inflammatory, Barrier Maintenance, and Gut Microbiome Modulation Effects of Saccharomyces cerevisiae QHNLD8L1 on DSS-Induced Ulcerative Colitis in Mice

“…According to a recent report, Faecalibaculum reduces inflammation by stimulating the development of Tregs in the colon, and a decrease in Faecalibaculum levels is associated with the emergence of colorectal cancer [ 52 ]. Hu et al [ 53 ] demonstrated that VK2 ameliorates DSS-induced colitis and reduces intestinal microflora dysbiosis by increasing Faecalibaculum and promoting SCFA production. The increased number of Faecalibaculum genera motivated a rise in the level of Butyricimonas , corroborating our finding that Faecalibaculum had a positive correlation with Butyricimonas .…”