3.2 TBⅡ prevented DSS-induced disruption of colonic epithelial
integrity and attenuated DSS-induced inflammation of colon tissue
One of the key features of DSS-induced colitis is the disruption of
colonic epithelial integrity and intestinal barrier homeostasis, and
thereby causing enhancing intestinal permeability and colonic and
systemic inflammatory infiltration. Given the alleviative effect of TBⅡ
in DSS-induced colitis, we then examine whether TBⅡ can ameliorate
DSS-induced the damage of colonic epithelial integrity. We demonstrated
a significant increase in intestinal permeability of FITC-dextran in
DSS-induced colitis mice compared with control mice, an effect that is
reduced by TBⅡ treatment (Figure 2A). Accordingly, the expression of
genes (such as E-cadherin and Occludin ) involved in
colonic tight junctions and adhesive junctions was increased after TBⅡ
treatment (Figure 2B). Consistently, the protein expression levels of
E-cadherin and Occludin determined by western blot, and
immunofluorescence were also elevated (Figure 2C and D).
Importantly, TBⅡ treatment also substantially diminished colonic
inflammatory infiltration, as revealed by reduced
F4/80+ positive cell recruitment to the colon tissue
and lower levels of MPO activity in plasma and colon tissue (Figure 2D
and E), a marker of inflammatory infiltration into the inflamed colon
tissue, and subsequently leading to abating colonic inflammation, as
seen by a decrease of pro-inflammatory cytokine release (TNF-α, IL-1β,
IL-6 and IL-10) (Figure 2F). Correspondingly, the expression of genes
associated colonic inflammation including TNF-α, IL-1β, IL-6 andIL-10 were prominently reversed in TBⅡ-treated colitis mice than
that of vehicle-treated DSS-induced colitis mice (Figure 2G).
Collectively, our results demonstrated that TBⅡ can alleviate
DSS-induced the disruption of colonic epithelial integrity via reducing
intestinal permeability and inflammatory infiltration.