An in vitro study on the regulation of oxidative protective genes in human gingival and intestinal epithelial cells after treatment with salmon protein hydrolysate peptides

Abstract

Background: Under physiological conditions, molecular oxygen generates reactive oxygen species (ROS) as metabolic by-products. In the absence of an adequate defense mechanism, the accumulation of ROS leads to cell membrane and DNA damage, in addition to tissue degeneration. The up/down regulation of one or more oxidative stress-related genes is one mechanism which confers cytoprotection to tissues exposed to oxidative injury. Objective: To measure the up/down regulation of 84 oxidative protective NRF2 genes within primary human gingival epithelial cells (HGEPp) and human intestinal epithelial cells (HIEC-6) when treated with varying concentrations of salmon protein hydrolysate (SPH) solution. Methods: We measured up/down regulation of 84 oxidative protective genes in primary human gingival epithelial pooled cells and human intestinal epithelial cells after pretreatment with 25, 50, and 100 μM/ml of salmon protein hydrolysate solution. A human RT2 Profiler PCR array was used to evaluate the relative change in the expression of these common oxidative protective genes. The salmon protein hydrolysate contains a mixture of bioactive peptides, resulting from enzyme hydrolysis of salmon head and backbones. Results: Treatment with salmon protein hydrolysate peptides demonstrated up-regulation for 16 human oxidative protective genes and down-regulation for 9 human oxidative stress-related genes. Three genes (ferritin heavy polypeptide-1 (FTH1), heme oxygenase-1 (HMOX1), and arachidonate 12-lipoxygenase (ALOX12)) showed regulation changes at physiologically applicable levels. Conclusion: The improved oxidation protection observed after SPH treatment conferred by HMOX1 / ALOX12 regulation to HGEPp and HIEC-6 cells may find ultimate utility for these bioactive peptides in the modulation of gastrointestinal stress in irritable bowel syndrome and enterocolitis.