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Oral Concurrent Session 3 - Basic Science

Oral Concurrent Sessions

(35) Potential mechanism of neuroprotection by magnesium sulfate and betamethasone in microglia and neural stem cells

Tuesday, February 13, 2024
2:00 PM - 2:15 PM  
Location: Potomac Ballroom D, Ballroom Level
Objective: The use of antepartum magnesium sulfate (MgSO4) and corticosteroids is associated with reductions in developmental disability among preterm infants. The protective mechanisms of these drugs remain unclear but may relate to neurodevelopment. As the brain grows in-utero, neural stem cells (NSCs) decline in number while microglia increase. We hypothesize that the mechanism of MgSO4/corticosteroids relate to drug interactions in these cells and their proportion within the fetal brain at the time of preterm birth. We aimed to characterize the neuroprotective actions of these drugs by evaluating cytokine production in stimulated human fetal microglia and NSCs in-vitro.

Study Design: Commercially available fetal derived microglia (HMC3) and NSCs (ReNcells) were given PBS as a control or stimulated for 24-hours with IL-1B, a mediator of perinatal neuroinflammatory injury. Cells were also given the vehicle, MgSO4, betamethasone (BTMZ) or MgSO4/BMTZ. The production of twelve cytokines/chemokines were compared in cell media collected 24-hours post exposure using a Milliplex immunology assay.

Results: In controls, cytokines/chemokines were absent or at low levels. With IL-1B exposure, the production of five cytokines/chemokines was elevated by NSCs (Figure 1) while microglia upregulated 11 of the 12 (Figure 2). Substantial production of pro-inflammatory IL-6 and IL-8 was observed by both cell types yet only microglia produced the anti-inflammatory cytokine IL-10. Treatment with MgSO4 but not BTMZ or MgSO4/BTMZ lowered IL-8 but not IL-6 in IL-1B exposed NSCs. For microglia, BTMZ alone and MgSO4/BTMZ reduced most cytokines upregulated by IL-1B.

Conclusion: In stimulated microglia and NSCs, proinflammatory cytokines were lowered selectively by each drug. BTMZ reduces inflammatory responses in microglia whereas NSCs are incrementally affected by MgSO4. Further research is needed to determine whether neuroprotection by these drugs relates to gestational age, as there are differences in the brain’s composition of microglia and NSCs at different times of exposure.