内毒素致兔急性肺损伤血红素加氧酶拮抗作用

Study on endotoxin-induced acute lung injury and antagonizing effect of heme oxygenase in rabbits

目的:探讨血红素加氧酶-1(HO-1)对内毒素致兔急性肺损伤(ALI)的保护作用。方法:将24只雄性新西兰白兔随机分为生理盐水对照组(A组),内毒素损伤组(B组),血晶素预处理组(C组)。用内毒素(700μg/kg)一次性静脉注射复制兔急性肺损伤模型。检测肺组织HO-1蛋白的表达情况,以及在实验前(0 h)、实验后0.5 h、1 h、2 h、4 h各点动脉血气、血清SOD值与MDA值。结果:B组动物静脉注射内毒素0.5 h后,动脉血氧分压下降至最低7.287kPa(<8kPa,符合急性肺损伤标准),血清SOD值2 h、4 h时明显低于A组(P<0.01),血清MDA值明显高于A组(P<0.01)。C组肺组织HO-1蛋白(平均光密度)明显高于A和B组(P<0.01)。结论:肺组织HO-1表达增加对内毒素所致ALI有一定的保护作用。

Objective：To clarify the protective effects of heme oxygenase in endotoxin-induced acute lung injury（ALl） in rabbits. Methods： Twenty four male New-Zealand rabbits were divided into three groups： control group A, endotoxin-treated group B and endotoxin plus hemin treated group C. ALI models of rabbits were replicated with intravascular endotoxin injection （ 700μg/kg）. The partial presser of oxygen, malondialdehyde（MDA） content and superoxide dismutase（SOD） activity in blood serum were measured before experiment（0 h） and after experiment 0.5 h, 1 h, 2 h and 4 h. HO-1 protein（ density mean） were measured in pulmonary tissue. Results ： After infusion of endotoxin, in group B, it was observed that the partial presser of oxygen decreased to 7. 287 kPa （ 〈 8 kPa） at 0. 5 h. The SOD activity in group B were obviously lower than those in group A （ P 〈 0.01 ） and MOD were higher than those in group A （P 〈 0.01 ） at 2 h and 4 h in experiment. HO-1 protein in pulmonary tissue in group C were higher than those both in group A and group B （ P 〈 0.01 ）. Conclusion ： The increased expression of HO-1 in pulmonary tissue has some protective effects on ALI induced by endotoxin.