Abstract
Background Cigarette smoke is a risk factor for Chronic Obstructive Pulmonary Disease (COPD). Given the lack of COPD curative treatment, dietary management for COPD patients has become important. This study investigated whether the medicinal foods (YT and RH) could suppress cigarette smoke exposure-induced inflammation and oxidative stress. Methods Chronic pulmonary inflammation in male C57 mice was induced by a 4-week exposure to cigarette smoke (CS). The medicinal foods YT and RH were orally administered 1 week prior to CS exposure. The protective effects were assessed by measuring the pulmonary function and histopathological evaluations. Inflammatory cell numbers and cytokines levels in BALF and blood serum were analyzed by enzyme-linked immunosorbent assay (ELISA). Malondialdehyde (MDA) and superoxide dismutase (SOD) levels of the lung were analyzed. Furthermore, the levels of phosphorylated ERK and NF-κB in both the mice lungs and RAW264.7 cells were also detected. Results YT and RH combination (YT + RH) significantly improved pulmonary function and suppressed the inflammation, including cell number and cytokines in BALF relative to the CS group; histological examination revealed protective effects of YT + RH in the lungs of mice exposed to CS. Moreover, the MDA level in the lung of the YT + RH group of mice was lower, the SOD activity was higher, and in vitro treatment of YT and RH combination attenuated reactive oxygen species (ROS) expression in mouse macrophage RAW264.7 cells stimulated with cigarette smoke (CSE). YT + RH combination significantly reduced the expression of pNF-κB and pERK in the lung tissues and macrophage stimulated with CSE. Conclusions YT and RH combination attenuates cigarette smoke-induced inflammation and oxidative stress through inhibition of the NF-κB/ERK signaling pathway.
Highlights
Cigarette smoke is a risk factor for Chronic Obstructive Pulmonary Disease (COPD)
Antibodies against pNF-κB p65 and HO-1 were purchased from Abcam Biotechnology (Cambridge, USA); antibodies against pERK, ERK and GAPDH were purchased from Cell Signaling Technology (MA, USA); H2DCFDA were purchased from ermo Fisher Scientific (MA, USA); the horseradish peroxidase- (HRP-)labeled goat antirabbit/mouse IgG (H + L) were purchased from Abcam Biotechnology (Cambridge, USA). e polyvinylidene fluoride (PVDF) membranes were obtained from Millipore Corporation (Billerica, USA)
Given that oxidation reactions induced by reactive oxygen species (ROS) are regarded as a trigger of the oxidative stress, we examined the effects of YT + RH on intracellular ROS production in RAW 264.7 cells
Summary
Cigarette smoke is a risk factor for Chronic Obstructive Pulmonary Disease (COPD). Given the lack of COPD curative treatment, dietary management for COPD patients has become important. is study investigated whether the medicinal foods (YT and RH) could suppress cigarette smoke exposure-induced inflammation and oxidative stress. Is study investigated whether the medicinal foods (YT and RH) could suppress cigarette smoke exposure-induced inflammation and oxidative stress. The MDA level in the lung of the YT + RH group of mice was lower, the SOD activity was higher, and in vitro treatment of YT and RH combination attenuated reactive oxygen species (ROS) expression in mouse macrophage RAW264.7 cells stimulated with cigarette smoke (CSE). Oxidative stress occurs when ROS is produced beyond the antioxidant capacity and damages the cellular components, such as DNA, lipids, and Evidence-Based Complementary and Alternative Medicine proteins Such damage could result in lung cell death, degradation of extracellular matrix, and loss of alveolar unit [9, 10]. A short-term protective effect of antioxidants on lung function was observed in two intervention studies in subjects with high exposure to oxidative air pollution under natural conditions [11]
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