Intestinal mucosal injury is associated with intestinal inflammation [
15]. We investigated whether AMD could ameliorate the inflammatory response in mice induced by LPS. A large number of studies suggest that the intestinal ischemia/reperfusion injury, LPS challenge, and intestinal inflammatory diseases can induce the expression of inflammatory cytokines in humans and animals [
16]. Both in vitro and in vivo studies show that over-secretory of inflammatory cytokines can have a negative effects on intestinal mucosal integrity, permeability and epithelial function of the intestinal mucosa [
17]. The imbalance of cytokine and chemokine secretion plays an important role in mucosal defense. IL-8 is produced by macrophages and epithelial cells. It can chemotaxis and activate neutrophils, which leads to mucous edema, leukocyte infiltration, increased vascular damage and permeability, resulting in immune inflammatory lesions [
18]. IL-4 can play a role in pro-inflammatory factors alone in the gut of mice, which can trigger inflammation [
19]. The study showed that LPS was identified by Toll like receptor 4 (TLR4) to release TNF-α, IL-1 beta and IL-6 and other cytokines, which mediate and promote the occurrence of inflammatory bowel disease (IBD) [
20]. Intraperitoneal injection of LPS can cause intestinal mucosal inflammation, which is characterized by increased inflammatory and anti-inflammatory cytokines. TNF-α plays a major role in causing intestinal inflammation, and its role is to accumulate inflammatory cells to the local tissues of the inflammation, cause edema, activate coagulation cascade, and form granuloma [
21]. The common way to treat IBD in clinic is to inhibit TNF-α by using TNF-α antagonist to improve and alleviate IBD symptoms. In this experiment, the mice were intraperitoneally injected with LPS to establish a model of intestinal injury in mice. LPS challenge increased the level of TNF-α, IL-1β, IL-4,IL-6 and IL-8 in the serum (Table
1). Importantly, AMD reduced the concentrations of TNF-α, IL-1β, IL-4,IL-6 and IL-8 in the serum, compared to LPS-challenged mice. These findings indicate that the AMD has beneficial effects in reducing intestinal mucosal inflammation. AMD may inhibit intestinal immune damage, reduce intestinal mucosal edema and promote intestinal mucosal repair by downregulating the expression of cytokine.
The structural characteristics of the small intestinal mucosa are circular folds, intestinal villi and microvilli. These characteristics greatly expand the surface area of the small intestine and make the nutrients fully digested and absorbed in the small intestine. The complete structure of the small intestine is the physiological basis of its digestion and absorption function, and its morphological and structural changes directly affect the surface area of villi, thereby affecting the body’s ability to absorb nutrients [
22]. The integrity and height of the intestinal villi determine the absorption area of the small intestine, the absorption of nutrients and the growth of the animals [
23]. Therefore, the increase of the villi height, the ratio of the villi/crypt or the decrease of the depth of the recess is related to the improvement of the digestion and absorption of nutrients [
24]. Compared with the LPS group, AMD increased the villus height and villus/crypt ratio of the duodenum, as well as the villus height and chorionic ratio of the jejunum and ileum. Crypt depth was significantly reduced in the duodenum and the jejunum, compared with the LPS group. The expression of inflammatory cytokines was consistent with the alteration in the structure of intestinal villi (Table
1). Based on these results, we concluded that AMD protected the intestinal mucosa from the LPS-induced injury.
AM is a well-known medicinal herb for reinforcing Qi (the vital energy) in traditional Chinese medicine [
25].
Astragalus polysaccharides has the characteristics of antioxidation [
26], immunomodulation [
27], antiviral, antitumor activities [
28] and cardiovascular protection [
29]. AM and its active components have been proved to be effective in the treatment of a variety of diseases, such as diabetes mellitus [
30] and cardiovascular disorders [
31]. In recent years, astragal’s polysaccharides effectively reduced the mucosal damage of experimental colitis in mice by shortening colonic length, reducing colon weight index, and reducing macroscopically and histological scores [
32], which is similar to the results of this experiment.