Abstract
Chronic obstructive pulmonary disease (COPD) is mainly caused by cigarette smoking (CS), with oxidative stress being one key component during its pathogenesis. This study aimed to investigate the effects of quercitrin (QE) on cigarette smoke extract (CSE)-induced cell apoptosis and oxidative stress in human bronchial epithelial cells (HBECs) and its underlying mechanism. HBECs were treated with 2% CSE for 24 h to establish in vitro COPD cellular models. CCK-8 assay and flow cytometry analysis were performed to evaluate cell viability and apoptosis, respectively. Western blotting was applied to examine protein levels and ELISA kits were used to examine contents of the indicated oxidant/antioxidant markers. The results demonstrated that CSE promoted apoptosis and suppressed viability of HBECs and QE reversed these effects. CSE caused increase in T-AOC, superoxide dismutase, and glutathione (GSH) peroxidase contents and decrease in MDA, reactive oxygen species , and GSH contents in HBECs, which were rescued by QE treatment. The CSE-induced Nrf2 nuclear translocation and elevation of NAD(P)H: quinone oxidoreductase 1 (NQO1) and heme oxygenase-1 (HO-1) expression were also reversed by QE in HBECs. The mitogen-activated protein kinase (MAPK) signaling was activated by CSE and further suppressed by QE in HBECs. Collectively, QE exerts a protective role in HBECs against cell apoptosis and oxidative damage via inactivation of the Nrf2/HO-1/NQO1 pathway and the MAPK/ERK pathway.
Highlights
It has been estimated that chronic obstructive pulmonary disease (COPD) ranks third among leading causes of mortality by 2020 [1]
We demonstrated the protective influence of QE on cigarette smoke extract (CSE)-induced apoptosis and oxidative stress in human bronchial epithelial cells (HBECs) via Nrf2 and mitogen-activated protein kinase (MAPK) pathways
We found that CSE promoted apoptosis and induced oxidant/antioxidant imbalance in HBECs, which were rescued by QE treatment
Summary
It has been estimated that chronic obstructive pulmonary disease (COPD) ranks third among leading causes of mortality by 2020 [1]. Oxidative stress refers to the imbalance of oxidation and antioxidation in the body attacked by harmful stimulating factors [5]. It can directly damage lung tissues and cause gene expression of proinflammatory mediator, exudation of inflammatory cells, and oxidative inactivation of protease, thereby facilitating the development of COPD [6]. Heme oxygenase-1 (HO-1) is a crucial endogenous enzyme that catalyzes heme decomposition and generates carbon monoxide, biliverdin, and ferrous iron to modulate apoptosis, inflammation, and oxidative stress [8]. NAD(P)H: quinone oxidoreductase 1 (NQO1) is a significant enzyme related to cell apoptosis and oxidative stress [9,10].
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