Abstract

Chronic obstructive pulmonary disease (COPD) is the major cause of morbidity and mortality worldwide, and cigarette smoke is a key factor in the development of COPD. Thus, the development of effective therapies to prevent the advancement of COPD has become increasingly essential. We hypothesized that quercetin protects lungs in mice exposed to long-term cigarette smoke. Thirty-five C57BL/6 mice were exposed to cigarette smoke (12 cigarettes per day) for 60 days and pretreated with 10 mg/kg/day of quercetin via orogastric gavage. After the experimental protocol, the animals were euthanized and samples were collected for histopathological, antioxidant defense, oxidative stress and inflammatory analysis. The animals exposed to cigarette smoke showed an increase in respiratory rate and hematological parameters, cell influx into the airways, oxidative damage and inflammatory mediators, besides presenting with alterations in the pulmonary histoarchitecture. The animals receiving 10 mg/kg/day of quercetin that were exposed to cigarette smoke presented a reduction in cellular influx, less oxidative damage, reduction in cytokine levels, improvement in the histological pattern and improvement in pulmonary emphysema compared to the group that was only exposed to cigarette smoke. These results suggest that quercetin may be an agent in preventing pulmonary emphysema induced by cigarette smoke.

Highlights

  • Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide, which caused 3 million deaths in 2019 [1]

  • Quercetin administration (QCSG) promoted a reduction in respiratory rate when compared to animals that were exposed to cigarette smoke (p = 0.01)

  • The cigarette smoke group showed higher values for red blood cell (ANOVA, p < 0.0001), hemoglobin (ANOVA, p < 0.0001) and hematocrit (ANOVA, p < 0.0001) analyses when compared to the groups exposed to ambient air (CG, vehicle group (VG), quercetin group (QG)) (p = 0.001)

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Summary

Introduction

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide, which caused 3 million deaths in 2019 [1]. Antioxidants 2022, 11, 181 recruitment of immune cells, mainly macrophages and neutrophils These cells maintain the inflammation process and increase ROS production, which in conjunction with the reactive species present in cigarette smoke can exceed the antioxidant capacity of the body, causing redox imbalance [7,8]. This imbalance is a major predisposing factor in the pathogenesis and progression of COPD. These processes lead to degradation of the extracellular matrix and consequent alveolar destruction [9,10]

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