Effect of soybean peptides against hydrogen peroxide induced oxidative stress in HepG2 cells via Nrf2 signaling.

Food Funct

Beijing Advanced Innovation Center for Food Nutrition and Human Health, Beijing Engineering and Technology Research Center of Food Additives, Beijing Technology and Business University (BTBU), Beijing 100048, China.

Published: March 2020

AI Article Synopsis

  • - The study investigated how soybean protein hydrolysates affect intracellular antioxidant activity by examining their impact on reactive oxygen species (ROS) production in HepG2 cells.
  • - Researchers extracted and sequenced soybean peptides and found that these peptides could inhibit ROS production while promoting the expression of antioxidant enzymes and the Nrf2 protein, which plays a key role in cellular defense against oxidative stress.
  • - The findings suggest that soybean peptides trigger a protective response by activating the Nrf2 pathway, enhancing the body's antioxidant capabilities, and potentially reducing oxidative damage.

Article Abstract

The aim of this study was to determine the effects of soybean protein hydrolysates against intracellular antioxidant activity. Soybean peptides (1000 to 2000 Da range) were extracted by soybean proteolysis and ultrafiltration and sequenced with a Nano-LC-ESI-MS/MS. In this study we found that soybean peptides inhibited the production of reactive oxygen species (ROS) induced by hydrogen peroxide (HO), malondialdehyde (MDA) and oxidized glutathione (GSSG) in HepG2 cells. Moreover, they also prevented the reduction of reduced glutathione (GSH) and up-regulated cellular resistance oxidase activity. In addition, soybean peptide treatment stimulated the mRNA and protein expression levels of antioxidant enzymes and nuclear factor erythroid-2-related factor 2 (Nrf2). Activated Nrf2 up-regulated antioxidant enzyme activities (superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px)) and inhibited ROS and MDA production. It was concluded that soybean peptides effectively activated the Nrf2/antioxidant response element (ARE) mediated activity.

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Source
http://dx.doi.org/10.1039/c9fo01466gDOI Listing

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