The neuroprotective effect of magnesium sulfate in preterm fetal mice

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)537-543
Number of pages7
JournalJournal of Perinatal Medicine
Volume43
Issue number5
DOIs
Publication statusPublished - 2015 Sep 1

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Magnesium Sulfate
Neuroprotective Agents
Sodium Chloride
Lipopolysaccharides
Inflammation
Premature Birth
Mifepristone
Intraperitoneal Injections
Confocal Microscopy
Brain Injuries
Therapeutics
Western Blotting
Immunohistochemistry

Keywords

  • Magnesium sulfate
  • mouse
  • Neun
  • preterm birth
  • S100B

ASJC Scopus subject areas

  • Obstetrics and Gynaecology
  • Pediatrics, Perinatology, and Child Health

Cite this

The neuroprotective effect of magnesium sulfate in preterm fetal mice. / Cho, Geum-Joon; Hong, Hye Ri; Hong, Soon Cheol; Oh, Min Jeong; Kim, Hai Joong.

In: Journal of Perinatal Medicine, Vol. 43, No. 5, 01.09.2015, p. 537-543.

Research output: Contribution to journalArticle

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abstract = "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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N2 - 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.

AB - 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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