Hyperoside Alleviates Helicobacter pylori-Induced Gastric Epithelial Cell Injury by Regulating Nrf2/HO-1 Signaling
Infection with is the major causative factor of chronic gastritis, peptic ulcer, gastric cancer, and other diseases. Gastric mucosal epithelial injury characterized by abnormal apoptosis, oxidative stress, and inflammation is a crucial mechanism of infection. Hyperoside (HYP) is a flavonol glycoside...
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| Published in | Polish journal of microbiology Vol. 74; no. 1; pp. 60 - 70 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
Poland
Sciendo
01.03.2025
De Gruyter Poland |
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| Online Access | Get full text |
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| Abstract | Infection with
is the major causative factor of chronic gastritis, peptic ulcer, gastric cancer, and other diseases. Gastric mucosal epithelial injury characterized by abnormal apoptosis, oxidative stress, and inflammation is a crucial mechanism of
infection. Hyperoside (HYP) is a flavonol glycoside derived from many herbal plants, which exhibits potent anti-apoptotic, antioxidant, and anti-inflammatory properties. Our research explored whether it exerts protective effects on
-infected human gastric epithelial cells. GES-1 cells were first treated for 24 h with HYP (0, 10, 20, 40, 80, 100, or 120 μM) to determine the cytotoxicity of HYP. Subsequently, GES-1 cells were pre-treated for 4 h with HYP (80 μM), followed by exposure to
for 24 h. CCK-8 assay, flow cytometry assay, ELISA, RT-qPCR, DCFH-DA staining, the commercial assay kits, immunofluorescence staining, and western blotting were used to assess cell viability, cell apoptosis, pro-inflammatory cytokine levels, oxidative stress marker levels, and Nrf2/HO-1 signaling-related molecule levels. The Nrf2 inhibitor ML385 was employed to verify the beneficial role of Nrf2 activation in HYP-mediated GES-1 cell injury induced by
. The results showed that HYP pre-treatment reversed
-induced cell apoptosis, inflammation, and oxidative stress in GES-1 cells. Furthermore, HYP downregulated Nrf2, HO-1, and NQO1 protein levels in
-infected GES-1 cells. ML385 overturned the protective effects of HYP against
-induced GES-1 cell apoptosis, inflammation, and oxidative stress. In conclusion, HYP protects gastric epithelial cells against
-induced cell injury by activating the Nrf2/HO-1 pathway. |
|---|---|
| AbstractList | Infection with Helicobacter pylori is the major causative factor of chronic gastritis, peptic ulcer, gastric cancer, and other diseases. Gastric mucosal epithelial injury characterized by abnormal apoptosis, oxidative stress, and inflammation is a crucial mechanism of H. pylori infection. Hyperoside (HYP) is a flavonol glycoside derived from many herbal plants, which exhibits potent anti-apoptotic, antioxidant, and anti-inflammatory properties. Our research explored whether it exerts protective effects on H. pylori-infected human gastric epithelial cells. GES-1 cells were first treated for 24 h with HYP (0, 10, 20, 40, 80, 100, or 120 μM) to determine the cytotoxicity of HYP. Subsequently, GES-1 cells were pre-treated for 4 h with HYP (80 μM), followed by exposure to H. pylori for 24 h. CCK-8 assay, flow cytometry assay, ELISA, RT-qPCR, DCFH-DA staining, the commercial assay kits, immunofluorescence staining, and western blotting were used to assess cell viability, cell apoptosis, pro-inflammatory cytokine levels, oxidative stress marker levels, and Nrf2/HO-1 signaling-related molecule levels. The Nrf2 inhibitor ML385 was employed to verify the beneficial role of Nrf2 activation in HYP-mediated GES-1 cell injury induced by H. pylori. The results showed that HYP pre-treatment reversed H. pylori-induced cell apoptosis, inflammation, and oxidative stress in GES-1 cells. Furthermore, HYP downregulated Nrf2, HO-1, and NQO1 protein levels in H. pylori-infected GES-1 cells. ML385 overturned the protective effects of HYP against H. pylori-induced GES-1 cell apoptosis, inflammation, and oxidative stress. In conclusion, HYP protects gastric epithelial cells against H. pylori-induced cell injury by activating the Nrf2/HO-1 pathway. Infection with Helicobacter pylori is the major causative factor of chronic gastritis, peptic ulcer, gastric cancer, and other diseases. Gastric mucosal epithelial injury characterized by abnormal apoptosis, oxidative stress, and inflammation is a crucial mechanism of H. pylori infection. Hyperoside (HYP) is a flavonol glycoside derived from many herbal plants, which exhibits potent anti-apoptotic, antioxidant, and anti-inflammatory properties. Our research explored whether it exerts protective effects on H. pylori -infected human gastric epithelial cells. GES-1 cells were first treated for 24 h with HYP (0, 10, 20, 40, 80, 100, or 120 μM) to determine the cytotoxicity of HYP. Subsequently, GES-1 cells were pre-treated for 4 h with HYP (80 μM), followed by exposure to H. pylori for 24 h. CCK-8 assay, flow cytometry assay, ELISA, RT-qPCR, DCFH-DA staining, the commercial assay kits, immunofluorescence staining, and western blotting were used to assess cell viability, cell apoptosis, pro-inflammatory cytokine levels, oxidative stress marker levels, and Nrf2/HO-1 signaling-related molecule levels. The Nrf2 inhibitor ML385 was employed to verify the beneficial role of Nrf2 activation in HYP-mediated GES-1 cell injury induced by H. pylori . The results showed that HYP pre-treatment reversed H. pylori -induced cell apoptosis, inflammation, and oxidative stress in GES-1 cells. Furthermore, HYP downregulated Nrf2, HO-1, and NQO1 protein levels in H. pylori -infected GES-1 cells. ML385 overturned the protective effects of HYP against H. pylori -induced GES-1 cell apoptosis, inflammation, and oxidative stress. In conclusion, HYP protects gastric epithelial cells against H. pylori -induced cell injury by activating the Nrf2/HO-1 pathway. Infection with is the major causative factor of chronic gastritis, peptic ulcer, gastric cancer, and other diseases. Gastric mucosal epithelial injury characterized by abnormal apoptosis, oxidative stress, and inflammation is a crucial mechanism of infection. Hyperoside (HYP) is a flavonol glycoside derived from many herbal plants, which exhibits potent anti-apoptotic, antioxidant, and anti-inflammatory properties. Our research explored whether it exerts protective effects on -infected human gastric epithelial cells. GES-1 cells were first treated for 24 h with HYP (0, 10, 20, 40, 80, 100, or 120 μM) to determine the cytotoxicity of HYP. Subsequently, GES-1 cells were pre-treated for 4 h with HYP (80 μM), followed by exposure to for 24 h. CCK-8 assay, flow cytometry assay, ELISA, RT-qPCR, DCFH-DA staining, the commercial assay kits, immunofluorescence staining, and western blotting were used to assess cell viability, cell apoptosis, pro-inflammatory cytokine levels, oxidative stress marker levels, and Nrf2/HO-1 signaling-related molecule levels. The Nrf2 inhibitor ML385 was employed to verify the beneficial role of Nrf2 activation in HYP-mediated GES-1 cell injury induced by . The results showed that HYP pre-treatment reversed -induced cell apoptosis, inflammation, and oxidative stress in GES-1 cells. Furthermore, HYP downregulated Nrf2, HO-1, and NQO1 protein levels in -infected GES-1 cells. ML385 overturned the protective effects of HYP against -induced GES-1 cell apoptosis, inflammation, and oxidative stress. In conclusion, HYP protects gastric epithelial cells against -induced cell injury by activating the Nrf2/HO-1 pathway. Infection with Helicobacter pylori is the major causative factor of chronic gastritis, peptic ulcer, gastric cancer, and other diseases. Gastric mucosal epithelial injury characterized by abnormal apoptosis, oxidative stress, and inflammation is a crucial mechanism of H. pylori infection. Hyperoside (HYP) is a flavonol glycoside derived from many herbal plants, which exhibits potent anti-apoptotic, antioxidant, and anti-inflammatory properties. Our research explored whether it exerts protective effects on H. pylori-infected human gastric epithelial cells. GES-1 cells were first treated for 24 h with HYP (0, 10, 20, 40, 80, 100, or 120 μM) to determine the cytotoxicity of HYP. Subsequently, GES-1 cells were pre-treated for 4 h with HYP (80 μM), followed by exposure to H. pylori for 24 h. CCK-8 assay, flow cytometry assay, ELISA, RT-qPCR, DCFH-DA staining, the commercial assay kits, immunofluorescence staining, and western blotting were used to assess cell viability, cell apoptosis, pro-inflammatory cytokine levels, oxidative stress marker levels, and Nrf2/HO-1 signaling-related molecule levels. The Nrf2 inhibitor ML385 was employed to verify the beneficial role of Nrf2 activation in HYP-mediated GES-1 cell injury induced by H. pylori. The results showed that HYP pre-treatment reversed H. pylori-induced cell apoptosis, inflammation, and oxidative stress in GES-1 cells. Furthermore, HYP downregulated Nrf2, HO-1, and NQO1 protein levels in H. pylori-infected GES-1 cells. ML385 overturned the protective effects of HYP against H. pylori-induced GES-1 cell apoptosis, inflammation, and oxidative stress. In conclusion, HYP protects gastric epithelial cells against H. pylori-induced cell injury by activating the Nrf2/HO-1 pathway.Infection with Helicobacter pylori is the major causative factor of chronic gastritis, peptic ulcer, gastric cancer, and other diseases. Gastric mucosal epithelial injury characterized by abnormal apoptosis, oxidative stress, and inflammation is a crucial mechanism of H. pylori infection. Hyperoside (HYP) is a flavonol glycoside derived from many herbal plants, which exhibits potent anti-apoptotic, antioxidant, and anti-inflammatory properties. Our research explored whether it exerts protective effects on H. pylori-infected human gastric epithelial cells. GES-1 cells were first treated for 24 h with HYP (0, 10, 20, 40, 80, 100, or 120 μM) to determine the cytotoxicity of HYP. Subsequently, GES-1 cells were pre-treated for 4 h with HYP (80 μM), followed by exposure to H. pylori for 24 h. CCK-8 assay, flow cytometry assay, ELISA, RT-qPCR, DCFH-DA staining, the commercial assay kits, immunofluorescence staining, and western blotting were used to assess cell viability, cell apoptosis, pro-inflammatory cytokine levels, oxidative stress marker levels, and Nrf2/HO-1 signaling-related molecule levels. The Nrf2 inhibitor ML385 was employed to verify the beneficial role of Nrf2 activation in HYP-mediated GES-1 cell injury induced by H. pylori. The results showed that HYP pre-treatment reversed H. pylori-induced cell apoptosis, inflammation, and oxidative stress in GES-1 cells. Furthermore, HYP downregulated Nrf2, HO-1, and NQO1 protein levels in H. pylori-infected GES-1 cells. ML385 overturned the protective effects of HYP against H. pylori-induced GES-1 cell apoptosis, inflammation, and oxidative stress. In conclusion, HYP protects gastric epithelial cells against H. pylori-induced cell injury by activating the Nrf2/HO-1 pathway. |
| Author | Zheng, Xiuhua Wang, Yanfen Liu, Yuxue |
| Author_xml | – sequence: 1 givenname: Yanfen surname: Wang fullname: Wang, Yanfen organization: Department of Basic Medicine, Henan Vocational College of Nursing, Anyang, China – sequence: 2 givenname: Yuxue surname: Liu fullname: Liu, Yuxue email: liuyuxue@htu.edu.cn organization: College of Life Science, Henan Normal University, Xinxiang, China – sequence: 3 givenname: Xiuhua surname: Zheng fullname: Zheng, Xiuhua organization: Department of Clinical Medicine, Henan Vocational College of Nursing, Anyang, China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40146790$$D View this record in MEDLINE/PubMed |
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| Keywords | Helicobacter pylori inflammation human gastric epithelial cells Hyperoside apoptosis gastritis oxidative stress |
| Language | English |
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| Snippet | Infection with
is the major causative factor of chronic gastritis, peptic ulcer, gastric cancer, and other diseases. Gastric mucosal epithelial injury... Infection with Helicobacter pylori is the major causative factor of chronic gastritis, peptic ulcer, gastric cancer, and other diseases. Gastric mucosal... Infection with Helicobacter pylori is the major causative factor of chronic gastritis, peptic ulcer, gastric cancer, and other diseases. Gastric mucosal... |
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| SubjectTerms | Anti-inflammatory agents Apoptosis Apoptosis - drug effects Assaying Cell activation Cell injury Cell Line Cell Survival - drug effects Cell viability Cholecystokinin Chronic infection Cytotoxicity Enzyme-linked immunosorbent assay Epithelial cells Epithelial Cells - drug effects Epithelial Cells - metabolism Epithelial Cells - microbiology Epithelium Flavonols Flow cytometry Gastric cancer Gastric mucosa Gastric Mucosa - drug effects Gastric Mucosa - microbiology Gastritis Glycosides Helicobacter Infections - drug therapy Helicobacter Infections - microbiology Helicobacter pylori Helicobacter pylori - drug effects Heme Oxygenase-1 - genetics Heme Oxygenase-1 - metabolism human gastric epithelial cells Humans Hyperoside Immunofluorescence Inflammation Injuries NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - metabolism NQO1 protein Original Paper Oxidative stress Oxidative Stress - drug effects Peptic ulcers Quercetin - analogs & derivatives Quercetin - pharmacology Signal Transduction - drug effects Staining Western blotting |
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| Title | Hyperoside Alleviates Helicobacter pylori-Induced Gastric Epithelial Cell Injury by Regulating Nrf2/HO-1 Signaling |
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