细菌内毒素增敏缺氧缺血性脑损伤动物模型的建立

Rat model of endotoxin sensitizing immature brain damage caused by hypoxia-ischemia

目的 :建立感染与HI联合作用引起脑损伤的动物模型 ,探讨细菌内毒素 (LPS)对缺氧缺血 (HI)引起脑损伤的增敏作用。方法 :7d龄新生大鼠给予不同剂量LPS ,观察动物体温、体重、脑损伤及病死率 ,确定亚临床感染的LPS剂量 ;亚临床感染剂量的LPS结合HI组和单纯HI对照组动物 ,在HI后 72h取脑进行微管相关蛋白 2 (MAP 2 )免疫组化染色 ,以评价 2组动物脑损伤程度。结果 :LPS 0 3mg/kg对新生大鼠无毒副作用 ,类似于亚临床感染。LPS 0 3mg/kg加HI10min时未见明显脑损伤 ,类似于单纯HI 10min的脑组织学改变 ;在LPS加HI 2 0min时 ,脑损伤程度明显大于对照组 ,与单纯HI 5 0min时的脑损伤程度类似。结论 :LPS 0 3mg/kg和单纯HI 2 0min均不能引起明显的脑损伤 ,二者联合作用却可以引起明显的脑损伤 。

Aim:To study the effect of endotoxin(LPS) on the immature brain and to establish brain damage model of infection combined with hypoxia ischemia(HI) Methods: Seven day old rat pups were injected subclinical dose LPS or normal saline,then subjected to hypoxia ischemia with different hypoxia time after 4 h injection The brains were taken at 72 h post HI MAP 2 immunostaining was used Results:LPS at the dosage of 0 3 mg/kg had no side effect on the neonatal rat pups After combination of LPS and HI, brain damage was found in 20 min group,but not in 10 min group,while no marked brain damage in the control group Conclusion: Both LPS at a dosage of 0 3 mg/kg and HI 20 min could not produce brain damage alone The pronounced brain damage can be produced by the combination of LPS and HI It's suggested that LPS sensitize the immature brain to hypoxia ischemia damage