To investigate the use of magnesium sulfate (MgSO<inf>4</inf>) 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 MgSO<inf>4</inf> or NS injection. From the 6 treatment groups (NS+NS, LPS+NS, NS+MgSO<inf>4</inf>, LPS+MgSO<inf>4</inf>, RU486+NS and RU486+MgSO<inf>4</inf>), 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+MgSO<inf>4</inf> group compared to the LPS+NS group. The expression of S100B did not differ between the RU486+NS and RU486+MgSO<inf>4</inf> groups. NeuN-labeled cells were increased in the LPS+MgSO<inf>4</inf> group compared with the LPS+NS group. NeuN-labeled cells were decreased in the RU486+MgSO<inf>4</inf> group compared with the RU486+NS group. Conclusions: We observed that prenatal treatment with MgSO<inf>4</inf> 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 MgSO<inf>4</inf> reduces inflammation-associated brain injury in fetal mice.
- Magnesium sulfate
- preterm birth
ASJC Scopus subject areas
- Obstetrics and Gynaecology
- Pediatrics, Perinatology, and Child Health