3.2 GP alleviates intestinal injury in rats with DSS-induced colitis.
DSS was used to establish an experimental model of rats with intestinal inflammation as described previously (Cosin-Roger et al., 2017; M. Zhou et al., 2018). HE stains clearly revealed that GP alleviated severe lesions in colon tissue, such as those that had histopathological characteristics of mucosal damage, necrosis, and inflammatory infiltration in DSS rats. Compared to the control group, the histological observation of the colon in the rats of model group demonstrated the inflammatory cell infiltration occurred in the mucosa. And the loss of goblet cells and epithelium, distorted crypts and the edema were also found in model group. After treatment in different doses of GP, the results showed the notable histologic improvements in the crypt architecture and the reductions in the edema, the mucosal injury and inflammatory infiltration. In the GP-H group, the histopathological properties of the colon of rats were improved most obviously, and ulcer healing lines appeared in some tissues (Fig. 2B). Furthermore, DSS-treated rats showed profound body weight loss, the change in body weights declined to 86.96% when compared to the initial weights. While GP treatment significantly attenuate the loss of body weight. Especially in the high-dose group of GP (DSS+GP-H), the change in body weights recover to 151.05% after 14 days of treatment (Fig. 2C). Rats in DSS+GP-L and DSS+GP-M groups also exhibited recovery of body weight to certain extent. These results demonstrated that DSS can successfully induce the intestinal inflammatory injury model in rats and High-dose of the GP treatment exerted the best curative effect in vivo. Therefore, the high-dose group of GP can be used for further studies to obtain more biological information, and the group of DSS+GP in the following refers to DSS+GP-H if not otherwise mentioned. Additionally, GP treatment also reversed DSS-induced inflammatory response, as evidenced by the spleen weight and the level of serum IL-1β, IL-8 and TNF-α (Fig. 2D, E, F and G).