Protective effect of soluble protein hydrolysate against H2O2‑induced intestinal injury: An interventional study

The present study aimed to investigate whether soluble protein hydrolysate (SPH) protects against intestinal oxidative stress injury. An <i>in vitro</i> lactate dehydrogenase assay was used to assess the cytotoxicity and protective effect of SPH. For <i>in vivo</i> assessment, friend virus B NIH Jackson mouse pups aged 21 days were administered with 5% w/v soluble protein hydrolysate (SPH) through drinking water for 14 days and then luminally injected with 0.3% or 0.6% H₂O₂. Thereafter, the fecal samples of mice were collected, and the mice were sacrificed. Intestinal epithelial injury was assessed, and the expressions of 84 oxidative stress‑related genes in intestinal tissues was determined. SPH prophylactically protected against H₂O₂‑induced oxidative stress injury in human intestinal epithelial cells. An animal model of oxidative stress‑induced intestinal injury was established using 0.3 and 0.6% H₂O₂. SPH treatment reduced oxidative stress (0.3% H₂O₂)‑induced gut injury in mice. As no accelerated body growth was observed in SPH‑treated mice, it was hypothesized that the underlying protective mechanism of SPH is not related to nutrient oversupply. Treatment with SPH upregulated five oxidative protective genes that were not consistent between the sexes. Some antioxidative genes, including ferritin heavy polypeptide‑1 (<i>Fth1</i>), heme oxygenase‑1 (<i>Hmox1</i>), NAD(P)H dehydrogenase quinone 1 (<i>Nqo1</i>) and superoxide dismutase 1 (<i>Sod1</i>), were commonly upregulated in both male and female mice. Overall, an antioxidative protective effect was observed following SPH treatment, which may be attributed to the upregulation of genes that protect against oxidative damage. The findings of the present study highlight the promising potential of SPH as a functional food for alleviating intestinal oxidative stress injury.