Wei Jingjing, Tao Guozhong, Liu Junlin, Framroze Bomi, Sylvester Karl G
Department of Surgery, Stanford University School of Medicine, Stanford, CA 94304, USA.
Department of R&D, Hofseth BioCare ASA, Aalesund 6003, Norway.
Mol Med Rep. 2025 Apr;31(4). doi: 10.3892/mmr.2025.13450. Epub 2025 Jan 31.
The present study aimed to investigate whether soluble protein hydrolysate (SPH) protects against intestinal oxidative stress injury. An lactate dehydrogenase assay was used to assess the cytotoxicity and protective effect of SPH. For 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% HO. 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 HO‑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% HO. SPH treatment reduced oxidative stress (0.3% HO)‑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 (), heme oxygenase‑1 (), NAD(P)H dehydrogenase quinone 1 () and superoxide dismutase 1 (), 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.
本研究旨在探讨可溶性蛋白水解物（SPH）是否能预防肠道氧化应激损伤。采用乳酸脱氢酶测定法评估SPH的细胞毒性和保护作用。为进行评估，给21日龄的Friend病毒B NIH Jackson幼鼠通过饮用水给予5% w/v的可溶性蛋白水解物（SPH），持续14天，然后经肠腔注射0.3%或0.6%的HO。此后，收集小鼠的粪便样本，并对小鼠实施安乐死。评估肠道上皮损伤，并测定肠道组织中84个氧化应激相关基因的表达。SPH预防性地保护了人肠道上皮细胞免受HO诱导的氧化应激损伤。使用0.3%和0.6%的HO建立了氧化应激诱导的肠道损伤动物模型。SPH治疗减轻了氧化应激（0.3% HO）诱导的小鼠肠道损伤。由于在接受SPH治疗的小鼠中未观察到体重加速增长，因此推测SPH的潜在保护机制与营养供应过剩无关。SPH处理上调了五个在性别间不一致的氧化保护基因。一些抗氧化基因，包括铁蛋白重链多肽-1（）、血红素加氧酶-1（）、NAD（P）H脱氢酶醌1（）和超氧化物歧化酶1（），在雄性和雌性小鼠中均普遍上调。总体而言，SPH处理后观察到抗氧化保护作用，这可能归因于保护免受氧化损伤的基因上调。本研究结果突出了SPH作为缓解肠道氧化应激损伤的功能性食品的潜在前景。
