中文摘要：

目的探讨氢气饱和生理盐水对内毒素（1ipopolysaccharide，LPS）诱导的小鼠急性肺损伤（acute lung injury，ALI）的保护作用。方法将90只雄性BABL／c小鼠随机分为空白（Sham）组、肺损伤（ALI）组、肺损伤氢气饱和生理盐水干预（ALI＋HRS）组，每组30只。Au组和ALI＋HRs组通过腹腔注射LPS制作肺损伤模型，ALI＋HRS组在LPS注射1h后，腹腔注射氢气饱和生理盐水，每组分别取12只小鼠，观察各组小鼠7d生存情况。在损伤后3、5、7d，每组处死3只小鼠，观察肺组织病理变化，检测肺组织中iNOS和Arg—1的表达变化。结果与Sham组相比，ALI组生存率降低；与ALI组相比，ALI＋HRS组生存率明显升高；H-E染色显示，与ALI组相比，ALI＋HRS组肺组织炎性细胞浸润明显减少；qPCR检测显示，相比于ALI组，ALI＋HRS组iNOS的表达量下降，Arg-1表达上升；免疫荧光染色的结果与qPCR相一致。结论对于LPS诱导的小鼠肺损伤，腹腔注射饱和氢气生理盐水能够抑制促炎因子iNOS的表达并促进抑炎因子Arg-1的表达，从而减轻内毒素诱导的小鼠肺损伤。

英文摘要：

Objective To evaluate the protective effect of hydrogen-rich saline （HRS） on lipopolysaccharide （LPS）-induced acute lung injury （ALl） in mice. Methods Ninety male BABL/c mice were randomly divided into Sham group, ALI group and ALl ＋ HRS group with 30 mice in each group. Acute lung injury model was induced by intraperitoneal injection of LPS in ALI and ALl ＋ HRS groups. Intraperitoneal injection of hydrogen-rich saline was given to mice in ALI＋ HRS group 1 h after injection of LPS. Twelve mice in each group were selected and observed for the 7 d-survival rate. Three mice in each group were sacrificed at the 3rd, 5th and 7th day after LPS injection, respectively. Pathological changes of the lungs were observed by H-E staining. The mRNA and protein expression of iNOS and Arg-1 in lung tissue was detected by qPCR and immunofluorescence staining, respectively. Results Compared with Sham group, the survival rate of ALI group was decreased; compared with ALl group, the survival rate of ALI＋ HRS group was significantly increased. H-E staining showed that the inflammatory cell infiltration in lung tissue of ALI ＋ HRS group was significantly decreased compared with ALI group, qPCR results showed that the expression of iNOS in ALI＋ HRS group decreased, and the expression of Arg~l increased compared with ALl group. The results of immunofluorescence staining were consistent with those of qPCR. Condusion Intraperitoneal injection of saturated hydrogen saline can inhibit the expression of proinflammatory factor iNOS and promote the expression of inflammatory factor Arg-1, which can reduce endotoxin induced lung injury in mice.