This is the first time that the effect of original CS against UC in mice has been reported and it is through promoting dominant intestinal microflora such as <i>Blautia</i>, mitigating intestinal microflora dysbiosis, and regulating the expressions of TNF-α, claudin-1, occludin, and ZO-1.
Meanwhile, MAP induced high specific antibody titers in vivo, reduced the DAI score, serum MPO activity, colorectal lymph node colony count, ultrastructural injuries, colon tissue histological index score and MPO activity in UC mice, while increasing the expression levels of occludin, claudin1 and ZO1 in colon tissues.
Patients with active and quiescent UC had upregulated expression of claudin-2 and reduced expression of occludin and ZO-1 compared to those of normal controls.
Consistent with these findings <i>in vitro</i>, we found that CAR overexpression could suppress gut inflammation, attenuate the downregulation of TJ protein ZO-1 and Occludin, and limit the induction of barrier permeability in a DSS induced ulcerative colitis rat model <i>in vivo</i>.