ArticleFrontiers in immunology2024
Green tea extract suppresses airway inflammation via oxidative stress-driven MAPKs/MMP-9 signaling in asthmatic mice and human airway epithelial cells.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Study on Comprehensive Quality Control of Herba Hyssopi Based on Chemical Components and Pharmacological Mechanism Action.Molecules (Basel, Switzerland) · 2026Article
- Natural medicines for asthma management: mechanisms aligned with endotypes and multi-dimensional intervention.Frontiers in pharmacology · 2026Review
- LYVE-1 identifies asthma and drives PDGF-BB-induced proliferation, migration, and oxidative stress in airway smooth muscle cells via the PI3K/Akt pathway.Frontiers in pharmacology · 2026Article
- Naturally derived bioactive compounds as regulators of oxidative stress and inflammation in asthma.Chinese medicine · 2025Review
- Article
- Titanium Dioxide Nanoparticle Exposure Provokes Greater Lung Inflammation in Females Than Males in the Context of Obesity.International journal of nanomedicine · 2025Article
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Authors and funding
10 authors.
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Abstract
Introduction: The anti-inflammatory effect of green tea extract (GTE) has been confirmed in asthmatic mice, however, the pharmacological mechanism is not fully elucidated. Methods: To investigate the therapeutic efficacy of GTE in asthma and identify specific pathways, murine model of allergic asthma was established by ovalbumin (OVA) sensitization and the challenge for 4 weeks, with oral treatment using GTE and dexamethasone (DEX). Inflammatory cell counts, cytokines, OVA-specific IgE, airway hyperreactivity, and antioxidant markers in the lung were evaluated. Also, pulmonary histopathological analysis and western blotting were performed. Results: The GTE100 and GTE400 groups showed a decrease in airway hyperresponsiveness and the number of inflammatory cells in the bronchoalveolar lavage fluid (BALF) compared to the OVA group. GTE treatment also reduced interleukin (IL)-13, IL-5, and IL-4 levels in the BALF, and OVA-specific immunoglobulin E levels in the serum compared to those in the OVA group. GTE treatment decreased OVA-induced mucus secretion and airway inflammation. In addition, GTE suppressed the oxidative stress, and phosphorylation of MAPKs, which generally occurs after exposure to OVA. GTE administration also reduced matrix metalloproteinase-9 activity and protein levels. Conclusion: GTE effectively inhibited asthmatic respiratory inflammation and mucus hyperproduction induced by OVA inhalation. These results suggest that GTE has the potential to be used for the treatment of asthma.
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