Inhibition of oxidative stress by apocynin attenuated chronic obstructive pulmonary disease progression and vascular injury by cigarette smoke exposure

Apocynin Endothelial Dysfunction
DOI: 10.1111/bph.16068 Publication Date: 2023-03-13T05:15:12Z
ABSTRACT
Background and Purpose Cardiovascular disease affects up to half of the patients with chronic obstructive pulmonary (COPD), exerting deleterious impact on health outcomes survivability. Vascular endothelial dysfunction marks onset cardiovascular disease. The present study examined effect a potent NADPH Oxidase (NOX) inhibitor free‐radical scavenger, apocynin, COPD‐related Experimental Approach Male BALB/c mice were exposed either room air (Sham) or cigarette smoke (CS) generated from 9 cigarettes·day −1 , 5 days week for 24 weeks without apocynin treatment (5 mg·kg ·day intraperitoneal injection). Key Results Eight‐weeks reduced airway neutrophil infiltration (by 42%) completely preserved function nitric oxide synthase (eNOS) availability against oxidative insults exposure. These preservative effects maintained until 24‐week time point. markedly inflammation (reduced macrophage, lymphocyte), lung decline (hyperinflation) prevented collagen deposition by Conclusion Implications Limiting NOX activity may slow COPD progression lower risk, particularly when signs stress become evident.
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