脂多糖可致敏高浓度氧对新生小鼠未成熟脑的损伤

Nan fang yi ke da xue xue bao = Journal of Southern Medical University(2014)

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Abstract
目的:探讨低浓度脂多糖(LPS)处理后高浓度氧对新生小鼠未成熟脑损伤的影响及其作用机制。方法48只PND3C57新生小鼠随机分为空气组、LPS处理组、高氧组、高氧+LPS组,采用LPS腹腔注射0.3 mg/kg,30 min后95%高浓度氧暴露24 h,LPS处理组、高氧组给予相应单因素处理,PND5断头取脑:(1)Tomato lectin免疫组化染色观测脑室周围白质小胶质细胞形态变化;(2)检测脑组织内脂质氧化物MDA含量;(3)Real-time PCR检测TNF-αmRNA表达变化;(4)Western-blot检测capsase-3蛋白表达。结果 Tomato lectin染色显示LPS组、高氧组及LPS+高氧组均可见脑室周围白质内小胶质细胞由静息态转化为激活态,高氧组激活的小胶质细胞数、脑内MDA含量、TNF-αmRNA表达、caspase-3蛋白表达均高于空气组、LPS组(P<0.05),LPS处理后高氧暴露(LPS+高氧组)能显著增强高氧暴露后的小胶质细胞活化效应(P<0.05)。结论高浓度氧暴露诱导小胶质细胞活化致未成熟脑损伤,低浓度LPS处理后能致敏上述效应。
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Key words
hyperoxia,lipopolysaccharide,neonatal mice,immature brain,microglia
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