Vitexin, one of the major active components in hawthorn,
has been
shown to possess multiple pharmacological activities. Here, we sought
to investigate the effect of vitexin on an ameliorating dextran sodium
sulfate (DSS)-induced ulcerative colitis (UC) mouse model and further
explored its potential mechanism. The results indicated that vitexin
administration could significantly alleviate the signs of colitis
via suppressing body weight loss, reducing disease activity index
(DAI) score, and mitigating colonic damage. Also, vitexin treatment
in colitis mice markedly inhibited the production of pro-inflammation
cytokines (such as IL-1β, IL-6, and TNF-α). Meanwhile,
vitexin also could markedly down-regulate the phosphorylation levels
of p65, IκB, and STAT1. Moreover, vitexin also dose-dependently
increased the expressions of muc-2, ZO-1, and occludin proteins in
colonic tissues of colitis mice. Further studies revealed that vitexin
dramatically modulated the disturbed intestinal flora in colitis mice.
Vitexin is beneficial for regulating abundances of some certain bacteria,
such as Bacteroides, Helicobacter, Alistipes, Lachnospiraceae_NK4A136_group, and Lachnospiraceae_UCG-006. Interestingly, the
correlation analysis indicated that key microbes were strongly correlated
with colitis features, such as pro-inflammatory cytokines and gut
barrier. Collectively, these results demonstrated that vitexin treatment
alleviated inflammation, intestinal barrier dysfunction, and intestinal
flora dysbiosis in colitis mice. Vitexin is expected to be a promising
compound for UC treatment.
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