Background:Asthma is a common cause of breathing difficulty in children and adults,and is characterized by chronic airway inflammation that is poorly controlled by available treatments.This results in severe disabilit...Background:Asthma is a common cause of breathing difficulty in children and adults,and is characterized by chronic airway inflammation that is poorly controlled by available treatments.This results in severe disability and applies a huge burden to the public health system.Methane has been demonstrated to function as a therapeutic agent in many diseases.The aim of the present study was to explore the effect of methane-rich saline(MRS)on the pathophysiology of a mouse model of asthma and its underlying mechanism.Methods:A murine model of ovalbumin(OVA)-induced allergic asthma was applied in this study.Mice were divided into three groups:a control group,an OVA group,and OVA-induced asthmatic mice treated with MRS as the third group.Lung resistance index(RI)and dynamic compliance(Cdyn)were measured to determine airway hyper-responsiveness(AHR).Haematoxylin and eosin(H&E)staining was performed and scored to show histopathological changes.Cell counts of bronchoalveolar lavage fluid(BALF)were recorded.Cytokines interleukin(IL)-4,IL-5,IL-13,tumor necrosis factorα(TNF-α),and C-X-C motif chemokine ligand 15(CXCL15)from BALF and serum were measured by enzyme-linked immunosorbent assay(ELISA).The oxidative stress indexes,including malondialdehyde(MDA),superoxide dismutase(SOD),catalase(CAT),glutathione(GSH),myeloperoxidase(MPO),and 8-hydroxydeoxyguanosine(8-OHdG),were determined using commercial kits.Apoptosis was evaluated by western blot,quantitative real-time polymerase chain reaction(qRT-PCR),and biochemical examination.Results:MRS administration reversed the OVA-induced AHR,attenuated the pathological inflammatory infiltration,and decreased the cytokines IL-4,IL-5,IL-13,TNF-α,and CXCL15 in serum and BALF.Moreover,following MRS administration,the oxidative stress was alleviated as indicated by decreased MDA,MPO,and 8-OHdG,and elevated SOD and GSH.In addition,MRS exhibited an anti-apoptotic effect in this model,protecting epithelial cells from damage.Conclusions:Methane improves pulmonary function and decreases infiltrative inflammatory cells in the allergic asthmatic mouse model.This may be associated with its anti-inflammatory,antioxidative,and anti-apoptotic properties.展开更多
基金Project supported by the National Natural Science Foundation of China(No.81371316)
文摘Background:Asthma is a common cause of breathing difficulty in children and adults,and is characterized by chronic airway inflammation that is poorly controlled by available treatments.This results in severe disability and applies a huge burden to the public health system.Methane has been demonstrated to function as a therapeutic agent in many diseases.The aim of the present study was to explore the effect of methane-rich saline(MRS)on the pathophysiology of a mouse model of asthma and its underlying mechanism.Methods:A murine model of ovalbumin(OVA)-induced allergic asthma was applied in this study.Mice were divided into three groups:a control group,an OVA group,and OVA-induced asthmatic mice treated with MRS as the third group.Lung resistance index(RI)and dynamic compliance(Cdyn)were measured to determine airway hyper-responsiveness(AHR).Haematoxylin and eosin(H&E)staining was performed and scored to show histopathological changes.Cell counts of bronchoalveolar lavage fluid(BALF)were recorded.Cytokines interleukin(IL)-4,IL-5,IL-13,tumor necrosis factorα(TNF-α),and C-X-C motif chemokine ligand 15(CXCL15)from BALF and serum were measured by enzyme-linked immunosorbent assay(ELISA).The oxidative stress indexes,including malondialdehyde(MDA),superoxide dismutase(SOD),catalase(CAT),glutathione(GSH),myeloperoxidase(MPO),and 8-hydroxydeoxyguanosine(8-OHdG),were determined using commercial kits.Apoptosis was evaluated by western blot,quantitative real-time polymerase chain reaction(qRT-PCR),and biochemical examination.Results:MRS administration reversed the OVA-induced AHR,attenuated the pathological inflammatory infiltration,and decreased the cytokines IL-4,IL-5,IL-13,TNF-α,and CXCL15 in serum and BALF.Moreover,following MRS administration,the oxidative stress was alleviated as indicated by decreased MDA,MPO,and 8-OHdG,and elevated SOD and GSH.In addition,MRS exhibited an anti-apoptotic effect in this model,protecting epithelial cells from damage.Conclusions:Methane improves pulmonary function and decreases infiltrative inflammatory cells in the allergic asthmatic mouse model.This may be associated with its anti-inflammatory,antioxidative,and anti-apoptotic properties.
