N,N-dimethylacetamide blocks inflammation-induced preterm birth and remediates maternal systemic immune responses.

ABSTRACT: The common excipient, N,N-dimethylacetamide (DMA), prevents imminent endotoxin-induced preterm birth in mice. The present study hypothesized that DMA forestalls preterm birth to term (defined as day 18.5 or later) by attenuating bacterial endotoxin lipopolysaccharide (LPS)-induced maternal systemic inflammatory responses and cervix remodeling. Accordingly, LPS (i.p.) on day 15 postbreeding stimulated preterm delivery within 24 h while mice treated with DMA 2 h preceding and 9 h following LPS administration remained pregnant, comparable to saline and DMA controls, to deliver viable pups at term. Irrespective of LPS or DMA + LPS treatment, maternal plasma pro- and anti-inflammatory cytokines on day 15.5 (12 h post-LPS) increased tenfold compared to baseline concentrations in controls. On day

SUBMITTER: Reznik SE 

PROVIDER: S-EPMC11893883 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature