Mechanical ventilation (MV) is a tool used for the treatment of patients with acute or chronic respiratory failure. However, MV is a non-physiological resource, and it can cause metabolic disorders such as release of pro-inflammatory cytokines and production of reactive oxygen species. In clinical setting, maneuvers such as sigh, are used to protect the lungs. Thus, this study aimed to evaluate the effects of sigh on oxidative stress and lung inflammation in healthy adult Wistar rats submitted to MV. Male Wistar rats were divided into four groups: control (CG), mechanical ventilation (MVG), MV set at 20 sighs/h (MVG20), and MV set at 40 sighs/h (MVG40). The MVG, MVG20, and MVG40 were submitted to MV for 1 h. After the protocol, all animals were euthanized and the blood, bronchoalveolar lavage fluid, and lungs were collected for subsequent analysis. In the arterial blood, MVG40 presented higher partial pressure of oxygen and lower partial pressure of carbon dioxide compared to control. The levels of bicarbonate in MVG20 were lower compared to CG. The neutrophil influx in bronchoalveolar lavage fluid was higher in the MVG compared to CG and MVG40. In the lung parenchyma, the lipid peroxidation was higher in MVG compared to CG, MVG20, and MVG40. Superoxide dismutase and catalase activity were higher in MVG compared to CG, MVG20, and MVG40. The levels of IL-1, IL-6, and TNF in the lung homogenate were higher in MVG compared to CG, MVG20, and MVG40. The use of sigh plays a protective role as it reduced redox imbalance and pulmonary inflammation caused by MV.

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.

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.