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.