Effect of hydrogen inhalation on mitochondrial biosynthesis in lung tissues during acute lung injury in mice with sepsis / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effect of hydrogen ( H2 ) inhalation on mitochondrial bio?synthesis in lung tissues during acute lung injury in mice with sepsis. Methods One hundred and four male ICR mice, aged 6 weeks, weighing 20-25 g, were divided into 4 groups ( n=26 each) using a ran?dom number table sham operation group ( group S) , sham operation + H2 group ( group S+H2 ) , sepsis group ( group Sep) and sepsis + H2 group ( group Sep+H2 ) . Sepsis was produced by cecal ligation and puncture. In S+H2 and Sep+H2 groups, the mice inhaled 2% H2 for 1 h starting from 1 and 6 h after opera?tion. Twenty mice in each group were selected, and the survival rates on postoperative days 1, 2, 3, 5 and 7 were recorded. On the postoperative day 1, 6 mice in each group were selected, and blood samples were collected from the common carotid artery for measurement of arterial oxygen partial pressure, and the oxygenation index was calculated. The pulmonary specimens were obtained for examination of the pathologi?cal changes which were scored and for determination of the expression of peroxisome proliferator?activated re?ceptor gamma coactivator?1α ( PGC?1α) in lung tissues by Western blot. The pulmonary mitochondria were isolated for determination of mitochndrial membrane potential ( MMP ) and ATP contents using spectropho?tometry and a bioluminescence technique, respectively. Results Compared with group S, the survival rate, oxygenation index and MMP and ATP content in lung tissues were significantly decreased, and the pathological scores and PGC?1α expression in lung tissues were significantly increased in Sep and Sep+H2 groups (P<0.05). Compared with group Sep, the survival rate, oxygenation index, and MMP, ATP content and PGC?1α expression in lung tissues were significantly increased, and the pathological scores were significantly decreased in group Sep+H2 ( P<0.05) . Conclusion H2 inhalation can ameliorate acute lung injury in mice with sepsis, and the mechanism is associated with the enhanced function of PGC?1αand promoted mitochondrial biosynthesis in lung tissues.