2. Academic Validation
  3. Alginate Oligosaccharides Protect Gastric Epithelial Cells against Oxidative Stress Damage through Induction of the Nrf2 Pathway

Alginate Oligosaccharides Protect Gastric Epithelial Cells against Oxidative Stress Damage through Induction of the Nrf2 Pathway

  • Antioxidants (Basel). 2024 May 20;13(5):618. doi: 10.3390/antiox13050618.
Samantha Acevedo 1,  Alejandra A Covarrubias 2 3,  Paola Haeger 4 5 6,  Floria Pancetti 2 6 7,  Fadia Tala 6 7 8 9,  Erwin de la Fuente-Ortega 1 6 7
Affiliations

Affiliations

  • 1 Laboratorio de Estrés Celular y Enfermedades Crónicas no Transmisibles, Universidad Católica del Norte, Coquimbo 1781421, Chile.
  • 2 Laboratorio de Neurotoxicología Ambiental, Departamento de Ciencias Biomédicas, Facultad de Medicina, Universidad Católica del Norte, Coquimbo 1781421, Chile.
  • 3 Facultad de Ciencias Agropecuarias, Universidad del Alba, La Serena 1700000, Chile.
  • 4 Laboratorio de Neurobiología de la Conducta, Departamento de Ciencias Biomédicas, Facultad de Medicina, Universidad Católica del Norte, Coquimbo 1781421, Chile.
  • 5 Millennium Nucleus of Neuroepigenetics and Plasticity (EpiNeuro), Santiago 8370186, Chile.
  • 6 Núcleo de Investigación en Prevención y Tratamiento de Enfermedades Crónicas no Transmisibles (NiPTEC), Universidad Católica del Norte, Coquimbo 1781421, Chile.
  • 7 Centro de Investigación y Desarrollo Tecnológico en Algas y Otros Recursos Biológicos (CIDTA), Facultad de Ciencias del Mar, Universidad Católica del Norte, Coquimbo 1781421, Chile.
  • 8 Departamento de Biología Marina, Facultad de Ciencias del Mar, Universidad Católica del Norte, Coquimbo 1781421, Chile.
  • 9 Instituto Milenio en Socio-Ecología Costera, SECOS, Santiago 7550000, Chile.
PMID: 38790723 DOI: 10.3390/antiox13050618
Abstract

Gastric diseases represent a significant global public health challenge, characterized by molecular dysregulation in redox homeostasis and heightened oxidative stress. Although prior preclinical studies have demonstrated the cytoprotective antioxidant effects of alginate oligosaccharides (AOSs) through the Nrf2 pathway, whether such mechanisms apply to gastric diseases remains unclear. In this study, we used the GES-1 gastric cell line exposed to hydrogen peroxide (H2O2) as a damage model to investigate the impact of AOS on cell viability and its associated mechanisms. Our results revealed that pre-incubation with AOS for either 4 h or 24 h significantly improved the viability of GES-1 cells exposed to H2O2. In addition, AOS reduced the intracellular ROS levels, activating the Nrf2 signaling pathway, with increased Nrf2 protein and mRNA expression and a significant upregulation of the target genes HO-1 and NQO1. The activation of Nrf2 was correlated with decreased Keap1 protein expression and an increased level of the Autophagy protein p62/SQSTM1, suggesting the activation of Nrf2 through a noncanonical pathway. This study suggests that AOS is a potential treatment for protecting gastric epithelial cells from oxidative stress by activating the p62/SQSTM1-Keap1-Nrf2 axis and laying the foundation for future investigations about its specific therapeutic mechanisms.

Keywords

AOS; GES-1; Keap1; Nrf2; alginate oligosaccharides; gastric diseases; p62/SQSTM1.

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