Journal of Southern Medical University ›› 2014, Vol. 34 ›› Issue (02): 214-.
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Abstract: Objective To explore the effect of low-concentration lipopolysaccharide (LPS) pretreatment on hyperoxia-inducedimmature brain injury in neonatal mice and explore and the related mechanisms. Methods Forty-eight neonatal mice onpostnatal day 3 (PND3) were randomized into normal control group, LPS (0.3 mg/kg) group, hyperoxia group (hyperoxiaexposure for 24 h), and hyperoxia+LPS group (hyperoxia exposure for 24 h 30 min after 0.3 mg/kg LPS treatment). At PND5,all the neonatal mice were sacrificed to examine the morphological changes of microglia in the periventricular white matterusing Tomato lectin staining, measure malondialdehyde (MDA) content in the immature brain, detect mRNA expression oftumor necrosis factor-α (TNF-α) using real-time PCR, and determine caspase-3 protein expression with Western blotting.Results Compared with the control group, exposures to LPS, hyperoxia, and both all resulted in microglia activation in theperiventricular white matter. The number of activated microglia, MDA content, TNF-α mRNA expression and caspase-3protein expression in the immature brain were significantly higher in hyperoxia group than in the control group and LPSgroup (P<0.05). LPS pretreatment significantly enhanced hyperoxia-induced microglia activation in the immature brain (P<0.05). Conclusion Hyperoxia causes immature brain injury mediated by microglia activation, and LPS pretreatment canenhance such brain injury in neonatal mice.
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https://www.j-smu.com/EN/Y2014/V34/I02/214