ArticleJournal of molecular neuroscience : MN2022
Fetal Neuroprotective Mechanism of Maternal Magnesium Sulfate: Proteomic Analysis.
Article in Journal of molecular neuroscience : MN, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Magnesium sulfate in oxidative stress-associated pathologies: clinical, cellular, and molecular perspectives.Biophysical reviews · 2025Review
- Intra-amniotic inflammation in the mid-trimester of pregnancy is a risk factor for neuropsychological disorders in childhood.Journal of perinatal medicine · 2023Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mg supplementation has been shown to protect preterm fetuses from white and gray matter damage, but the mechanism is unclear. The purpose of this study was to study the effect of maternal inflammation on the overall protein panel of the fetal rat brain, as well as the neuroprotective effect of magnesium-sulfate (MG). Pregnant rats at e20 (n = 6, 18 total) received injections of i.p. lipopolysaccharide (LPS) 500 ug/kg or control saline (SAL) at time 0. Dams were randomized to treatment with s.c. MG (270 mg/kg loading followed by 27 mg/kg q20 min) or saline (SAL) from -2 to +2 h, followed by an additional injection of MG (270 mg/kg) at +2 h. At 4 h after LPS administration, fetal brains were collected from the 3 treatment groups (LPS/SAL, LPS/MG, SAL/SAL) and analyzed by proteomic technique. LPS significantly decreased fetal brain complement C3, alpha-1-antiproteinase, metallothionein-3, alpha-2-macroglobulin, neurosecretory protein VGF, glutathione S-transferase mu 2, fam91a1, cnot7, mitogen-activated protein kinase levels, and significantly increased fetal brain Hbg1, while MG treatment normalized these measures to normal values. Maternal inflammation may cause brain injury via pathways other than the activation of neurotoxic cytokines; this effect could be due to increased/decreased production of certain proteins associated with securing oligodendrocytes, encouraging neuronal growth in the brain, or protecting against cerebral ischemia. MG's neuroprotective activity may be achieved by modifying the effect of LPS on proteins involved in early brain development.
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