Magnesium sulfate reduces inflammation-associated brain injury in fetal mice

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.

Key words: inflammation, magnesium sulfate, mouse model, neuronal injury, preterm birth