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.%目的：评价吸入氢气对脓毒症小鼠急性肺损伤时肺组织线粒体生物合成的影响。方法雄性ICR小鼠104只，6周龄，体重20～25 g，采用随机数字表法，将其分为4组（ n＝26）：假手术组（ S组）、假手术＋氢气组（ S＋H2组）、脓毒症组（ Sep组）和脓毒症＋氢气组（ Sep＋H2组）。采用盲肠结扎穿孔法制备小鼠脓毒症模型，于术后1、6 h时S＋H2组和Sep＋H2组分别吸入2％氢气，时间均为1h。每组取20只小鼠，记录术后1、2、3、5、7d时生存情况；术后1d时每组取6只小鼠，采集颈总动脉血样，测定PaO2，计算氧合指数；然后取肺组织，行肺组织病理学评分；分离肺组织线粒体，采用分光光度法检测线粒体膜电位（ MMP ），采用萤光素⁃荧光酶发光法检测线粒体ATP含量，采用Western blot法测定肺组织过氧化物酶体增殖物激活受体γ辅激活因子⁃1α（ PGC⁃1α）表达。结果与S组比较，Sep组和Sep＋H2组生存率、氧合指数、肺组织MMP和ATP含量降低，肺组织病理学评分升高，肺组织PGC⁃1α表达上调（ P＜0．05）；与Sep组比较，Sep＋H2组生存率、氧合指数、肺组织MMP、ATP含量升高，肺组织PGC⁃1α表达上调，肺组织病理学评分降低（ P＜0．05）。结论吸入氢气可减轻脓毒症小鼠急性肺损伤，其机制与增强肺组织PGC⁃1α功能，促进线粒体生物合成有关。
展开▼
