In Vitro Protective Effect of Pea‐Derived Peptides (PPs) via the Keap1/Nrf2 Signaling Pathway on Alpha‐Gliadin‐Sensitizing Peptide Induced Cacao‐2 Cells

Author:

Gao Bing1,Cui Chenxu2ORCID,Yan Fang1,Li Ning3,Sun Xuefeng2,Wang Fangyu2ORCID,Wang Chunfeng1

Affiliation:

1. The First Affiliated Hospital of Zhengzhou University 1# Mianfang Street Zhengzhou 450052 China

2. Henan Key Laboratory of Animal Immunology Henan Academy of Agricultural Sciences 116# Huayuan Road Zhengzhou Henan Province 450002 China

3. School of Food Science and Technology Henan Agricultural University 63#Agricultural Road Zhengzhou 450000 PR China

Abstract

ScopeCeliac disease (CD) is an allergic intestinal disease caused mainly by gliadin in wheat, which is widespread in the population and currently lacks effective treatment. α‐Gliadin peptides cause cellular damage by substantially increasing cellular reactive oxygen species (ROS) levels.Methods and resultsThis study investigates the protective effect of 11 pea‐derived peptides (PPs) on ɑ‐gliadin peptide (P31‐43) treated Caco‐2 cells. Results show that cells treated with PP2, PP5, and PP6 peptides significantly reduce the cell mortality caused by P31‐43. Three PPs significantly reduce the P31‐43‐induced decrease in ROS levels to control levels, and there is no difference between them and the vitamin C (Vc) group. The results in terms of antioxidant‐related enzymes show that PPs significantly decrease superoxide dismutase activity (SOD), glutathione reductases (GR), and glutathione (GSH)/oxidized glutathione (GSSG) levels, thus significantly enhancing the antioxidant level of cells. By studying the key proteins of the Kelch‐like ECH‐associated protein 1 (Keap1)/NF‐E2‐related factor 2 (Nrf2) pathway, it is found that PPs activate the Keap1/Nrf2 signaling pathway.ConclusionThe study finds that peptides from peas can effectively alleviate ɑ‐gliadin peptide‐induced cell damage. The discovery of these food‐derived peptides provides novel potential solutions for the prevention and treatment of CD.

Publisher

Wiley

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