AB4 attenuates DSS-induced colon injury
The increased permeability in the intestinal epithelium is an important
indicator that the mechanical barrier function of the intestinal mucosa
is impaired (Sommer et al., 2021). Next, we further evaluated the
protective effect of AB4 on DSS-induced colitis. FITC-dextran assay of
intestinal permeability in mice showed that the diffusion of
FITC-dextran across the epithelium was significantly lower in AB4
administration mice (Fig. 2A). This supported the conclusion that AB4
reduced DSS-induced intestinal mucosal injury in mice. Intestinal
barrier function is maintained by tight junction proteins, such as
Occludin, Claudin-1, and ZO-1 (Sommer et al., 2021). Compared with the
DSS group, AB4 (5, 10, and 15mg/kg) significantly enhanced the
expression of Occludin, Claudin-1, and ZO-1 proteins (Fig. 2B), which
was consistent with the FITC-dextran results. Hematoxylin and eosin
(H&E) staining indicated that AB4 (5, 10, and 15 mg/kg) markedly
alleviated mucosal damage, infiltration of inflammatory cells, and loss
of
crypts
(Fig.
2C). AB4 decreased histological colon damage score compared to the DSS
group (Fig. 2C). Consistently, AB4
(5,
10, and 15 mg/kg) significantly abolished the distribution of
F4/80+ macrophages in colonic lamina propria (Fig.
2D). Thus, AB4 attenuated the severity of DSS-induced colonic injury in
mice.