Effect of hydrogen on lipopolysaccharide-induced acute lung injury in mice
Objective To investigate the mechanism of hydrogen alleviating lipopolysaccharide(LPS)-induced acute lung injury in mice.Methods The mice were randomly divided into four groups:control group(group C),hydrogen inhalation group(group H),lung injury model group(group L)and lung injury model+hydrogen inhalation group(group LH),3 mice in each group.Group C was not treated,and the acute lung injury model was established by intraperitoneal injection of LPS 10 mg/kg in groups L and LH.After the successful preparation of the lung injury model,the group LH received hydrogen interven-tion.Pulmonary edema was detected by pulmonary ultrasound 12 hours after modeling,then mice were sacri-ficed promptly.The left lung tissue was used to detect the protein of p-AMPK,p-ERK and p-p38.The right lung tissues were observed by HE staining for lung histopathological changes and lung injury score.Results Compared with group C,the B-line area in groups L and LH was significantly increased,and the protein contents of p-AMPK,p-ERK,and p-p38 were significantly increased(P<0.05),the protein contents of P-AMPK in group H was significantly increased(P<0.05),the lung injury score in group L was signifi-cantly increased(P<0.05).Compared with the group L,the B-line area,p-ERK,p-ERK and p-p38 pro-tein contents and lung injury score in group LH were significantly decreased(P<0.05).The lung tissue of groups C and H had no red blood cell leakage,no edema,no inflammatory cell infiltration,and the struc-ture was clearly visible.The group L showed a large number of red blood cell leakage,inflammatory cell in-filtration and pulmonary interstitial edema and thickening.Lung bleeding,inflammatory cell infiltration,and thickening of alveolar septa were reduced in the group LH.Conclusion Hydrogen alleviates endotoxin-in-duced lung injury in mice,possibly related to the upregulation of p-AMPK and downregulation of p-ERK/p-p38 expressions.
HydrogenLipopolysaccharideAcute lung injuryMitogen-activated protein kinases