Biochemical and biophysical research communications · 2026
Integrated bioinformatics and ex-vivo evaluation of resveratrol in modulating oxidative stress and neutrophil extracellular traps in COPD.
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Kumar Anshu, Das Sarvjeet, Koirala Nabin, Khatua Debnarayan, Kshatriya Ravish, Jyoti Anupam
Аннотация
BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease characterized by persistent inflammation and oxidative stress-mediated pathogenesis. Identifying patient-specific drug targeting oxidative damage is of paramount importance. Resveratrol has emerged as a promising therapeutic candidate owing to its antioxidant and anti-inflammatory properties. This study aims to identify its targets and evaluate its therapeutic efficacy in neutrophil-driven oxidative stress in COPD.
METHODS: Bioinformatic analyses were performed using the GSE11952 and GSE232805 datasets. Top-ranked hub genes were identified for candidate drug screening and validated through molecular docking. Human peripheral blood neutrophils from healthy volunteers as well as COPD patients were isolated and challenged with bacteria or PMA, with or without resveratrol, under ex-vivo cigarette smoke exposure (CSE) followed by Python-based statistical and exploratory data analyses. We further assessed the effects of resveratrol on reactive oxygen species (ROS) generation and neutrophil extracellular traps (NETs) formation.
RESULTS: The top-ranked identified hub genes common across the three centrality algorithms were FN1, CD44, ITGA5, and THBS1, having roles in extracellular matrix-receptor interaction, advanced glycation end-products-receptor, hypoxia-inducible factor 1, cytokine signalling, and ferroptosis pathways. Molecular docking results demonstrated the highest binding affinity between resveratrol and ITGA5 (-7.4 kcal/mol). Ex-vivo quantitative analysis revealed that resveratrol significantly attenuated bacterial-induced ROS in healthy and CSE neutrophils. Additionally, it showed significant efficacy in reducing ROS and NET formation in PMA-stimulated neutrophils of COPD patients.
CONCLUSION: Resveratrol exerted a significant antioxidant effect in modulating oxidative stress in COPD. Integrated bioinformatics and ex-vivo experiments suggest that ITGA5 may be a candidate target through which Resveratrol suppressed ROS generation and NETs formation in COPD.
METHODS: Bioinformatic analyses were performed using the GSE11952 and GSE232805 datasets. Top-ranked hub genes were identified for candidate drug screening and validated through molecular docking. Human peripheral blood neutrophils from healthy volunteers as well as COPD patients were isolated and challenged with bacteria or PMA, with or without resveratrol, under ex-vivo cigarette smoke exposure (CSE) followed by Python-based statistical and exploratory data analyses. We further assessed the effects of resveratrol on reactive oxygen species (ROS) generation and neutrophil extracellular traps (NETs) formation.
RESULTS: The top-ranked identified hub genes common across the three centrality algorithms were FN1, CD44, ITGA5, and THBS1, having roles in extracellular matrix-receptor interaction, advanced glycation end-products-receptor, hypoxia-inducible factor 1, cytokine signalling, and ferroptosis pathways. Molecular docking results demonstrated the highest binding affinity between resveratrol and ITGA5 (-7.4 kcal/mol). Ex-vivo quantitative analysis revealed that resveratrol significantly attenuated bacterial-induced ROS in healthy and CSE neutrophils. Additionally, it showed significant efficacy in reducing ROS and NET formation in PMA-stimulated neutrophils of COPD patients.
CONCLUSION: Resveratrol exerted a significant antioxidant effect in modulating oxidative stress in COPD. Integrated bioinformatics and ex-vivo experiments suggest that ITGA5 may be a candidate target through which Resveratrol suppressed ROS generation and NETs formation in COPD.