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).