Abstract

Cigarette smoke is highly toxic, and it can promote increased production of reactive species and inflammatory response and leads to liver diseases. Quercetin is a flavonoid that displays antioxidant and anti-inflammatory activities in liver diseases. This study aimed at evaluating the protective effects of quercetin on livers from mice exposed to long-term cigarette smoke exposure. Male C57BL/6 mice were divided into five groups: control (CG), vehicle (VG), quercetin (QG), cigarette smoke (CSG), quercetin, and cigarette smoke (QCSG). CSG and QCSG were exposed to cigarette smoke for sixty consecutive days; at the end of the exposures, all animals were euthanized. Mice that received quercetin daily and were exposed to cigarette smoke showed a reduced influx of inflammatory cells, oxidative stress, inflammatory reaction, and histopathological changes in the liver, compared to CSG. These results suggest that quercetin may be an effective adjuvant for treating damage to the liver due to cigarette smoke exposure.

Highlights

  • Cigarette smoking is considered one of the leading preventable causes of morbidity and mortality representing a risk factor for several diseases such as cardiovascular, chronic obstructive pulmonary, and liver diseases [1, 2]

  • The mice were divided into 5 groups (n = 8 per group): a control group exposed to ambient air (CG), a group that received 200 μL of vehicle solution containing 50% propylene glycol (Sigma Aldrich, Missouri, USA) and 50% saline (VG) by orogastric gavage, a group that received 10 mg/kg/day of quercetin (Sigma Aldrich, Missouri, USA) diluted in 200 μL of propylene glycol solution (QG), a group exposed to cigarette smoke (CSG), and a group administered with quercetin and exposed to cigarette smoke (QCSG)

  • There was a decrease of the final body weight (ANOVA, p < 0:0001) of the CSG compared to CG and VG (p = 0:001)

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Summary

Introduction

Cigarette smoking is considered one of the leading preventable causes of morbidity and mortality representing a risk factor for several diseases such as cardiovascular, chronic obstructive pulmonary, and liver diseases [1, 2]. Cigarette smoke (CS) is a highly toxic complex mixture of components containing more than 5000 compounds that can promote damage to biological tissues [3]. The CS produces reactive oxygen species (ROS) that, at high concentrations, brings about changes in the redox process and induction of inflammatory responses, triggering several comorbidities [4,5,6]. The exposure to cigarette smoke causes damage to cells and tissues by developing oxidative processes. The installation of oxidative stress can occur directly through the production of ROS or by the activation of the inflammatory process, which, in turn, results in an increased level of radical species [7, 8]

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