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Inhibition of oxidative stress by apocynin attenuated COPD progression and vascular injury by cigarette smoke exposure
  • +12
  • Stanley Chan,
  • Kurt Brassington,
  • Suleman Almerdasi,
  • Aleksandar Dobric,
  • Simone De Luca,
  • Madison Coward-Smith,
  • Hao Wang,
  • Kevin Mou,
  • Alina Akhtar,
  • Rana Alateeq,
  • Wei Wang,
  • Huei Seow,
  • Stavros Selemidis,
  • Steven Bozinovski,
  • Ross Vlahos
Stanley Chan
RMIT University
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Kurt Brassington
RMIT University College of Science Engineering and Health
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Suleman Almerdasi
RMIT University
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Aleksandar Dobric
RMIT University
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Simone De Luca
RMIT University
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Madison Coward-Smith
RMIT University
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Hao Wang
RMIT University
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Kevin Mou
RMIT University
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Alina Akhtar
RMIT University
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Rana Alateeq
RMIT University
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Wei Wang
RMIT University
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Huei Seow
RMIT University
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Stavros Selemidis
RMIT University
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Steven Bozinovski
RMIT University
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Ross Vlahos
RMIT University

Corresponding Author:[email protected]

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Abstract

Background and Purpose: Cardiovascular disease (CVD) affects up to half of the patients with chronic obstructive pulmonary disease (COPD), which exerts deleterious impact on health outcomes and survivability. Vascular endothelial dysfunction marks the onset of cardiovascular disease. The present study examined the effect of a potent NADPH Oxidase (NOX) inhibitor and free-radical scavenger, apocynin, on COPD-related CVD. Experimental Approach: Male BALB/c mice were exposed to either room air (Sham) or cigarette smoke (CS) generated from 9 cigarettes per day, 5 days a week for up to 24 weeks with or without apocynin treatment (5 mg·kg-1·day-1, intraperitoneal injection). Key Results: Eight-weeks of apocynin treatment reduced airway neutrophil infiltration (by 42%) and completely preserved endothelial function and endothelial nitric oxide synthase (eNOS) activity against the oxidative insults of CS exposure. These preservative effects were maintained up until the 24-week time point. 24-week of apocynin treatment exhibited marked benefits on airway inflammation (reduced infiltration of macrophage, neutrophil and lymphocyte) and lung function decline (hyperinflation), and prevented airway collagen deposition by CS exposure. Conclusion and Implications: Limiting NOX activity may slow COPD progression and lower CVD risk, particularly when signs of oxidative stress become evident.
13 Dec 2022Submitted to British Journal of Pharmacology
14 Dec 2022Submission Checks Completed
14 Dec 2022Assigned to Editor
14 Dec 2022Review(s) Completed, Editorial Evaluation Pending
18 Dec 2022Reviewer(s) Assigned
27 Jan 2023Editorial Decision: Revise Minor
06 Feb 20231st Revision Received
08 Feb 2023Submission Checks Completed
08 Feb 2023Assigned to Editor
08 Feb 2023Review(s) Completed, Editorial Evaluation Pending
08 Feb 2023Reviewer(s) Assigned
07 Mar 2023Editorial Decision: Accept