More than 50% of the world population is infected with Helicobacter pylori (H. pylori), which is classified as group I carcinogen by the WHO. H. pylori surface adhesins specifically recognize gastric mucosal epithelial cells’ (GES-1 cells) receptor to complete the adhesion. Blocking the adhesion with an anti-adhesion compound is an effective way to prevent H. pylori infection. The present study found that corn protein hydrolysate, hydrolyzed by Neutral, effectively alleviated gastric injury induced by H. pylori infection through anti-adhesive and anti-inflammatory effects in vitro and in vivo. The hydrolysate inhibited H. pylori adhesion to GES-1 cells significantly, and its anti-adhesive activity was 50.44 ± 0.27% at 4 mg/mL, which indicated that the hydrolysate possessed a similar structure to the GES-1 cells’ receptor, and exhibited anti-adhesive activity in binding to H. pylori. In vivo, compared with the H. pylori infection model group, the medium and high dose of the hydrolysate (400–600 mg/kg·bw) significantly decreased (p < 0.05) the amount of H. pylori colonization, pro-inflammatory cytokines (IL-6, IL-1β, TNF-α and MPO), chemokines (KC and MCP-1) as well as key metabolites of NF-κB signaling pathway levels (TLR4, MyD88 and NF-κB), and it increased antioxidant enzyme contents (SOD and GSH-Px) and the mitigation of H. pylori-induced pathological changes in the gastric mucosa. Taken together, these results indicated that the hydrolysate intervention can prevent H. pylori-induced gastric injury by anti-adhesive activity and inhibiting the NF-κB signaling pathway’s induction of inflammation. Hence, the corn protein hydrolysate might act as a potential anti-adhesive agent to prevent H. pylori infection.
Objectives: This study aimed to clarify the effect of lactic acid bacteria-fermented corn protein hydrolysate (FCH) on fatigue in mice and explore the connection between fatigue-related indicators and intestinal microbial flora. Methods: The fatigue model of mice was constructed by exercise endurance experiment. The anti-fatigue level of FCH was evaluated by measuring physiological and biochemical indexes in mouse serum, liver and skeletal muscle. The relationship between FCH, intestinal flora and fatigue was explored through the analysis of intestinal microbial diversity in mice, and the anti-fatigue mechanism of FCH was further analyzed. Results: The results showed that the weight-bearing swimming time of mice was prolonged by 1.96 times, and the running time of mice was prolonged by 2.63 times in the high-dose FCH (FCH-H) group. Moreover, the lactic acid contents in the blood were reduced by 16.00%, and lactate dehydrogenase activity and urea nitrogen contents basically returned to the normal level. Meanwhile, the malondialdehyde contents were reduced by 31.24%, and superoxide dismutase activity and glutathione contents were increased by 1.84 times and 1.72 times, respectively. In addition, the glycogen contents of the body were restored, and the muscle glycogen and liver glycogen were increased by 1.81 and 5.81 times, respectively. Analysis of intestinal microbial flora diversity in mice showed that the highest relative abundance was Lactobacillus, and the FCH group could recover and even increase its relative abundance. Lactobacillus was significantly positively correlated with muscle glycogen and SOD. Conclusions: FCH can alleviate fatigue by regulating fatigue-related indicators and improving the intestinal microbial flora of the organism.