Objective: To investigate the use of magnesium sulfate (MgSO4) as a neuroprotective agent in a mouse model of inflammation-associated and noninflammation-associated preterm birth.
Methods: On embryonic day 15 of gestation, lipopolysaccharide (LPS) and mifepristone (RU486) were used, respectively, to create mouse models of inflammation and noninflammation-associated preterm birth. After intraperitoneal injection of LPS, RU486, or normal saline solution (NS), dams were randomized to intraperitoneal MgSO4 or NS injection. From the 6 treatment groups (NS+NS, LPS+NS, NS+MgSO4, LPS+MgSO4, RU486+NS and RU486+MgSO4), fetal brains were collected for Western blot analysis and neuronal cultures. Protein expression of S100B was assessed, and immunohistochemistry was performed to detect NeuN. The numbers of NeuN-labeled cells were counted using confocal laser scanning microscopy.
Results: The expression of S100B significantly differed among the groups and was decreased in the LPS+MgSO4 group compared to the LPS+NS group. The expression of S100B did not differ between the RU486+NS and RU486+MgSO4 groups. NeuN-labeled cells were increased in the LPS+MgSO4 group compared with the LPS+NS group. NeuN-labeled cells were decreased in the RU486+MgSO4 group compared with the RU486+NS group.
Conclusions: We observed that prenatal treatment with MgSO4 was associated with decreased expression of S100B and increased numbers of NeuN-labeled cells in an inflammation-associated preterm mouse model but not in a noninflammation-associated preterm mouse model. Our results suggest that prenatal treatment of MgSO4 reduces inflammation-associated brain injury in fetal mice.
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