Effects of hydrogen gas on myocardial injury in rats with endotoxemia
10.3760/cma.j.issn.0254-1416.2012.07.031
- VernacularTitle:氢气对内毒素血症大鼠心肌损伤的影响
- Author:
Ling LIU
;
Xinwei LIU
;
Canxin LIANG
;
Dongwei HE
;
Ying YU
- Publication Type:Journal Article
- Keywords:
Hydrogen;
Toxemia;
Myocardium
- From:
Chinese Journal of Anesthesiology
2012;32(7):883-885
- CountryChina
- Language:Chinese
-
Abstract:
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.
