目的评价吸入氢气对脓毒症小鼠急性肺损伤时炎性反应的影响。方法雄性ICR小鼠48只,体重20~25g,5周龄,采用随机数字表法,将其随机分为4组(n=12):假手术组(A组)、假手术+氢气组(B组)、脓毒症组(c组)和脓毒症+氢气组(D组)。采用盲肠结扎穿孔(cLP)法制备脓毒症模型。B组和D组于假手术或CLP后1、6h吸入2%氢气1h。CLP后24h时行行为学评分,随后采集动脉血行血气分析,计算氧合指数;采集静脉血样,随后处死小鼠取肺组织,测定血清及肺组织TNF—α、IL-1β、高迁移率族蛋白B1(HMGB1)和IL-10水平和计算凋亡指数。结果与A组比较,C组和D组行为学评分升高,氧合指数降低,凋亡指数升高,血清及肺组织TNF-α、IL-1β、HMGB1和IL-10水平升高(P〈0.05),B组差异无统计学意义(P〉0.05);与C组比较,D组行为学评分降低,氧合指数升高,凋亡指数降低,血清及肺组织TNF-α、IL-1β和HMGB1水平降低,IL-10水平升高(P〈0.05)。结论吸人氢气可调节促炎和抗炎因子水平平衡,抑制炎性反应,减轻脓毒症小鼠急性肺损伤。
Objective To investigate the effect of inhalation of hydrogen (H2 ) on the inflammation re- sponse during sepsis-induced acute lung injury in mice. Methods Forty-eight male ICR mice, aged 5 weeks, weighing 20-25 g, were randomly divided into 4 groups ( n = 12 each) : sham operation group (group A), sham operation + H2 group (group B), sepsis group (group C) and sepsis + H2 group (group D). Sepsis was pro- duced by cecal ligation and puncture (CLP) . Groups B and D received 1 h inhalation of 2% H2 at 1 and 6 h after CLP or sham operation. The behavior was assessed and scored at 24 h after CLP. Arterial blood samples were tak- en for blood gas analysis. Oxygenation index was calculated. Venous blood samples were taken for determination of the levels of serum tumor necrosis factor-α (TNF-α), interleukin-I (IL-1β), high mobility group protein B1 (HMGB1) and interleukin-10 (IL-10). The mice were then sacrificed and lungs were removed for determination of the levels of TNF-a, IL-1β, HMGB1 and IL-10 in lung tissues. The apoptotic index was calculated. Results Compared with group A, the behavior score, apoptotic index and levels of TNF-a, IL-1β, HMGB1 and IL-10 were increased, and the oxygenation index was decreased in groups C and D, and no significant change was found in the parameters mentioned above in group B. Compare with group C, the oxygenation index and level of IL-10 were sig- nificantly increased, and the behavior score, apoptotic index and levels of TNF-α, IL-1β and HMGBI were signifi- cantly decreased in group D. Conclusion Inhalation of H2 can regulate the balance between pro- and anti-inflam- matory eytokines, inhibit the inflammation response and alleviate sepsis-induced acute lung injury in mice.