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Hyperoside Alleviates Helicobacter pylori-Induced Gastric Epithelial Cell Injury by Regulating Nrf2/HO-1 Signaling

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26 mar 2025

Hyperoside Alleviates Helicobacter pylori-Induced Gastric Epithelial Cell Injury by Regulating Nrf2/HO-1 Signaling's Cover Image

Polish Journal of Microbiology

Volumen 74 (2025): Edición 1 (Marzo 2025)

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Categoría del artículo: ORIGINAL PAPER

Publicado en línea: 26 mar 2025

Páginas: 60 - 70

Recibido: 14 jun 2024

Aceptado: 08 ene 2025

DOI: https://doi.org/10.33073/pjm-2025-005

Palabras clave
Hyperoside, gastritis, human gastric epithelial cells, inflammation, oxidative stress, apoptosis

© 2025 Yanfen Wang et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

HYP reduces Helicobacter pylori-induced GES-1 cell apoptosis.
A)Assessment of GES-1 cell viability after 24 h treatment with HYP (0, 10, 20, 40, 80, 100, or 120 μM) by CCK-8 assay;
B)evaluation of the viability of H. pylori-infected GES-1 cells pre-treated with or without HYP (80 μM) by CCK-8 assay;
C)analysis of GES-1 cell apoptosis following HYP pre-treatment and H. pylori stimulation through flow cytometry assay;
D–E)measurement of Bax and Bcl-2 protein levels in H. pylori-infected GES-1 cells with or without HYP pre-treatment via western blotting. *p < 0.05, ***p < 0.001 vs. control; ##p < 0.01, ###p < 0.001 vs. H. pylori. — HYP reduces Helicobacter pylori-induced GES-1 cell apoptosis. A)Assessment of GES-1 cell viability after 24 h treatment with HYP (0, 10, 20, 40, 80, 100, or 120 μM) by CCK-8 assay; B)evaluation of the viability of H. pylori-infected GES-1 cells pre-treated with or without HYP (80 μM) by CCK-8 assay; C)analysis of GES-1 cell apoptosis following HYP pre-treatment and H. pylori stimulation through flow cytometry assay; D–E)measurement of Bax and Bcl-2 protein levels in H. pylori-infected GES-1 cells with or without HYP pre-treatment via western blotting. *p < 0.05, ***p < 0.001 vs. control; ##p < 0.01, ###p < 0.001 vs. H. pylori.

HYP mitigates Helicobacter pylori-induced GES-1 cell inflammation. GES-1 cells were pre-treated with HYP for 4 h (80 μM), followed by H. pylori infection for 24 h.
A–C)Detection of TNF-α, IL-6, and IL-1β levels in GES-1 cell supernatants by ELISA;
D–F)analysis of TNF-α, IL-6, and IL-1β mRNA levels in GES-1 cells through RT-qPCR. ***p < 0.001 vs. control; ###p < 0.001 vs. H. pylori. — HYP mitigates Helicobacter pylori-induced GES-1 cell inflammation. GES-1 cells were pre-treated with HYP for 4 h (80 μM), followed by H. pylori infection for 24 h. A–C)Detection of TNF-α, IL-6, and IL-1β levels in GES-1 cell supernatants by ELISA; D–F)analysis of TNF-α, IL-6, and IL-1β mRNA levels in GES-1 cells through RT-qPCR. ***p < 0.001 vs. control; ###p < 0.001 vs. H. pylori.

HYP ameliorates Helicobacter pylori-induced oxidative stress in GES-1 cells. GES-1 cells were pre-treated with HYP for 4 h (80 μM), followed by H. pylori infection for 24 h.
A)Measurement of DCF fluorescence intensity in GES-1 cells using flow cytometry;
B)quantification of intracellular ROS production by measuring DCF fluorescence intensity;
C–E)examination of MDA content and SOD and CAT activities in GES-1 cells using the corresponding assay kits. **p < 0.01, ***p < 0.001 vs. control; #p < 0.05, ##p < 0.01, ###p < 0.001 vs. H. pylori. — HYP ameliorates Helicobacter pylori-induced oxidative stress in GES-1 cells. GES-1 cells were pre-treated with HYP for 4 h (80 μM), followed by H. pylori infection for 24 h. A)Measurement of DCF fluorescence intensity in GES-1 cells using flow cytometry; B)quantification of intracellular ROS production by measuring DCF fluorescence intensity; C–E)examination of MDA content and SOD and CAT activities in GES-1 cells using the corresponding assay kits. **p < 0.01, ***p < 0.001 vs. control; #p < 0.05, ##p < 0.01, ###p < 0.001 vs. H. pylori.

HYP activates the Nrf2/HO-1 signaling in Helicobacter pylori-infected GES-1 cells. GES-1 cells were pre-treated with HYP (80 μM) for 4 h, followed by H. pylori infection for 24 h.

A–D)Determination of Nrf2, HO-1, and NQO1 protein levels in GES-1 cells by western blotting. ***p < 0.001 versus control; ###p < 0.001 versus H. pylori;
E)representative immunofluorescence staining images showing Nrf2 expression (green) in GES-1 cells. Nuclei were stained with DAPI (blue);
F–I)estimation of Nrf2, HO-1, and NQO1 protein levels in GES-1 cells that were pre-treated with HYP (80 μM) and ML385 (5 μM) for 4 h before infection with H. pylori through western blotting. **p < 0.01, ***p < 0.001 vs. H. pylori; ###p < 0.001 vs. H. pylori + HYP. — HYP activates the Nrf2/HO-1 signaling in Helicobacter pylori-infected GES-1 cells. GES-1 cells were pre-treated with HYP (80 μM) for 4 h, followed by H. pylori infection for 24 h. A–D)Determination of Nrf2, HO-1, and NQO1 protein levels in GES-1 cells by western blotting. ***p < 0.001 versus control; ###p < 0.001 versus H. pylori; E)representative immunofluorescence staining images showing Nrf2 expression (green) in GES-1 cells. Nuclei were stained with DAPI (blue); F–I)estimation of Nrf2, HO-1, and NQO1 protein levels in GES-1 cells that were pre-treated with HYP (80 μM) and ML385 (5 μM) for 4 h before infection with H. pylori through western blotting. **p < 0.01, ***p < 0.001 vs. H. pylori; ###p < 0.001 vs. H. pylori + HYP.

The Nrf2 inhibitor ML385 reverses Helicobacter pylori-induced GES-1 cell injury. GES-1 cells were pre-treated with HYP (80 μM) and ML385 (5 μM) for 4 h before infection with H. pylori.

A)Evaluation of GES-1 cell apoptosis using flow cytometry assay; B)–C) examination of Bax and Bcl-2 protein levels in GES-1 cells through western blotting;
D)–F)analysis of TNF-α, IL-6, and IL-1β mRNA levels in GES-1 cells via RT-qPCR; G) assessment of DCF fluorescence intensity in GES-1 cells using flow cytometry; H) quantification of intracellular ROS production by measuring DCF fluorescence intensity. **p < 0.01, ***p < 0.001 vs. H. pylori; #p < 0.05, ###p < 0.001 versus H. pylori + HYP. — The Nrf2 inhibitor ML385 reverses Helicobacter pylori-induced GES-1 cell injury. GES-1 cells were pre-treated with HYP (80 μM) and ML385 (5 μM) for 4 h before infection with H. pylori. A)Evaluation of GES-1 cell apoptosis using flow cytometry assay; B)–C) examination of Bax and Bcl-2 protein levels in GES-1 cells through western blotting; D)–F)analysis of TNF-α, IL-6, and IL-1β mRNA levels in GES-1 cells via RT-qPCR; G) assessment of DCF fluorescence intensity in GES-1 cells using flow cytometry; H) quantification of intracellular ROS production by measuring DCF fluorescence intensity. **p < 0.01, ***p < 0.001 vs. H. pylori; #p < 0.05, ###p < 0.001 versus H. pylori + HYP.

Idioma:: Inglés

Calendario de la edición:: 4 veces al año
Temas de la revista:: Ciencias de la vida, Microbiología y virología

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