沐舒坦对盐酸吸入后大鼠氧化抗氧化系统的影响

目的：观察沐舒坦对盐酸吸入性肺损伤是否具有保护作用，并探讨其可能机制。方法：30只健康SD大鼠随机分成3组（A组：生理盐水吸入组；B组：稀盐酸吸入组；C组：稀盐酸吸入＋沐舒坦处理组）。C组予以50 mg/kg沐舒坦腹腔注射，每天1次，连续3 d，A，B组则以等体积生理盐水腹腔注射代替。第3 d腹腔注射沐舒坦或生理盐水30 min后，A组以1.2 ml/kg生理盐水经气管注入作为对照组；B，C组用pH 1.25盐酸+生理盐水混合液1.2 ml/kg气管注入。观察盐酸注入5 h后大鼠动脉血气、肺组织匀浆和血清中SOD活力、MDA含量。结果：沐舒坦预先处理能抑制盐酸吸入后引起的PaO2下降，3组间比较差异有统计学意义（P<0.01）。盐酸吸入5 h后B组肺匀浆和血中SOD活力均明显下降、肺匀浆MDA升高，而C组在盐酸吸入5 h后肺匀浆以及血中SOD活力明显高于B组，肺匀浆MDA则比B组明显低（P<0.01）,但3组血中MDA值比较差异无统计学意义（P>0.05）。结论：沐舒坦对盐酸吸入性肺损伤有保护作用，抑制脂质过氧化反应、提高抗氧化能力可能是沐舒坦减轻盐酸吸入性肺损伤的机制之一。

Oxidative and anti-oxidative effects of ambroxol on acute hydrochloric acid-induced lung injury in rats

Objective To evaluate the protective effect of ambroxol on acute hydrochloric acid- induced lung injury in rats. Methods Thirty pathogen-free SD rats were randomly divided into 3 groups: Group A (n=10) served as control group, and received intracheal instillation of normal saline (NS, pH5.3,1.2 ml/kg) with pre-treatment of intraperitoneal NS;Group B (n=10)received intracheal instillation of hydrochloric acid /NS (pH1.25,1.2 ml/kg) with pre-treatment of intraperitoneal NS; and Group C received intracheal instillation of hydrochloric acid /NS (pH1.25,1.2 ml/kg) with pre-treatment of intraperitoneal ambroxol (50 mg/kg/d, 3 days). Five hours after the instillation of the injury vehicle, the arterial gas was examined, the levels of superoxide dismutase (SOD), malondialdehyde(MDA) in the blood and homogenate of harvested lung were assayed respectively. Results PaO 2 in Group B was significantly lower than that in Group A and C (P<0.01),and pH and PaCO 2 in the 3 groups had little difference (P>0.05).MDA in the lungs of Group B increased obviously,and levels of SOD in the lung and blood decreased significantly in Group B (Group B vs Group A,P<0.01).Levels of SOD of Group C in the lung and blood were markedly higher than those of Group B (P<0.01),MDA of Group C was obviously lower than that of Group B (P<0.01),and MDA of blood in the 3 groups had no significant difference (P>0.05).Conclusion Ambroxol can inhibit lipid peroxidation and increase antioxidant activity, which may be one of the mechanisms in protecting lung tissue from hydrochloric acid-induced injury.