期刊
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
卷 202, 期 3, 页码 -出版社
MOSBY-ELSEVIER
DOI: 10.1016/j.ajog.2010.01.022
关键词
inflammation; magnesium sulfate; mouse model; neuronal injury; preterm birth
资金
- NICHD NIH HHS [R01 HD046544-05, R01 HD046544, 5-R01-HD046544-0] Funding Source: Medline
OBJECTIVE: The purpose of this study was to investigate whether magnesium sulfate (MgSO4) prevents fetal brain injury in inflammation-associated preterm birth (PTB). STUDY DESIGN: Using a mouse model of PTB, lipopolysaccharide (LPS) or normal saline solution (NS)-exposed mice were randomized to intraperitoneal treatment with MgSO4 or NS by intrauterine injection. From the 4 treatment groups (NS + NS; LPS + NS; LPS + MgSO4; and NS + MgSO4), fetal brains were collected for quantitative polymerase chain reaction studies and primary neuronal cultures. Messenger RNA expression of cytokines, cell death, and markers of neuronal and glial differentiation were assessed. Immunocytochemistry and confocal microscopy were performed. RESULTS: There was no difference between the LPS + NS and LPS + MgSO4 groups in the expression of proinflammatory cytokines, cell death markers, and markers of prooligodendrocyte and astrocyte development (P>.05 for all). Neuronal cultures from the LPS + NS group demonstrated morphologic changes; this neuronal injury was prevented by MgSO4 (P<.001). CONCLUSION: Amelioration of neuronal injury in inflammation-associated PTB may be a key mechanism by which MgSO4 prevents cerebral palsy.
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