Objective To investigate the effects of hydrogen gas on the myocardial injury in rats with endotoxemia.Methods Forty-eight healthy male Sprague-Dawley rats,weighing 200-220 g,were randomly divided into 4 groups (n =12 each ):control group (group C ),hydrogen gas control group (group HC ),endotoxemia group (group E) and hydrogen gas + endotoxemia group (group LH).Endotoxemia was induced by intraperitoneal lipopolysaccharide (LPS) 20 mg/kg in groups E and LH,while the equal volume of normal saline was given in groups C and HC.After LPS administration,the rats were exposed to the air containing 2％ hydrogen gas for 6 h in groups HC and LH,and the rats were exposed to the air for 6 h in groups C and E.Blood samples were taken from the abdominal aorta after 6 h inhalation of hydrogen gas to determine the serum level of cTnI.The hearts were then removed to determine the content of TNF-α and IL-6 and expression of phosphorylated nuclear factor κB ( NF-κB) inhibitory protein (p-IκB-α) and p38 mitogen-activated protein kinase (p-p38MAPK) in the myocardial tissues.Results Compared with group C,no significant change was found in the levels of cTnI,TNF-α and IL-6 and expression of p-IκB-α and p-p38MAPK in group HC ( P ＞ 0.05),and the levels of cTnI,TNF-α and IL-6 were significantly increased and the expression of p-IκB-α and p-p38MAPK was up-regulated in groups E and LH ( P ＜ 0.05).Compared with group E,the levels of cTnI,TNF-α and IL-6 were significantly decreased and the expression of p-IκB-α and p-p38MAPK was down-regulated in group LH ( P ＜ 0.05).Conclusion Hydrogen gas can reduce the myocardial injury in rats with endotoxemia,and inhibition of the p38MAPK and NF-κB pro-inflammatory pathway and reduction of the inflammatory response of myocardial tissues are involved in the mechanism.

OBJECTIVETo investigate the effect of hydrogen inhalation on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and the underlying molecular mechanisms.

METHODSThirty-two male SD rats were randomly divided into 4 groups (n=8), namely the normal saline group (SA), saline with 2% hydrogen gas inhalation group (SH group), ALI group, and ALI with hydrogen inhalation group (LH group). In the two ALI groups, ALI was induced by intraperitoneal injection of 15 mg/kg LPS. Treatments with inhalation of 2% hydrogen gas for 6 h was administered after the injection of LPS or saline. The concentrations of tumor necrosis factor-α (TNF-α) in the lung tissue and serum were examined with ELISA. The expression of p38 MAPK in the lung tissue was detected by Western blotting..

RESULTSHydrogen inhalation decreased the expression of p-p38 MAPK in the lung tissue, and significantly reduced TNF-α content in the lung tissue and serum of rats with ALI.

CONCLUSIONHydrogen inhalation can decrease the expression of TNF-α in the lung tissue and serum, and this effect may be related with reduced p38 MAPK expression and inhibition of p38 MAPK activation.

Acute Lung Injury ; blood ; chemically induced ; metabolism ; Administration, Inhalation ; Animals ; Hydrogen ; administration & dosage ; Lipopolysaccharides ; Lung ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; blood ; metabolism ; p38 Mitogen-Activated Protein Kinases ; blood ; metabolism