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Intrauterine growth restriction (IUGR) increases the risk of preterm birth and both are associated with enhanced inflammatory response. We sought to investigate whether magnesium attenuates inflammatory cytokines in a rat model of IUGR.
Pregnant female Wistar rats (12 wks old, GD18) were divided in four groups: normal diet with bilateral uterine artery ligation (BL; n=6) or sham surgery (SH; n=5); and magnesium chloride 1% in drinking water throughout gestation + BL: MgBL (n=5) or sham: MgSH (n=5). Dams were euthanized 24 hrs postsurgery (GD19). We collected: maternal plasma, fetal plasma (pooled from a single dam), individual amniotic fluid samples, and placentas from live fetal pups only (BL=36; SH=20; MgBL=20; MgSH=20). All samples were analyzed for cytokines (IL-6, IL-1β, CXCL1, CCL2 and TNFα; sensitivity <3pg/ml) using multiplex. Data was analyzed using ANOVA and t-test.
The average fetal and placental weights were significantly lower in the BL dams when compared to SH dams (P<0.001) (Table 1) . The overall fetal mortality was not significantly different for BL vs. MgBL. The incidence of IUGR (Pup weight <10th) in BL vs. MgBL were 86.3% vs. 31% respectively [RR: 0.36 (CI:0.2-0.6) P <0.0001]. IL-6, IL-1β, TNFα (P<0.05) and CCL2 (P<0.001) levels were significantly increased in the BL amniotic fluids, while IL-6, IL-1β, CCL2 and CXCL1 (P<0.001) and TNFα (P<0.05) were significantly increased in BL placental tissues when compared to SH, magnesium supplementation decreased the cytokine expression of IL-1β, TNFα and CCL2 in amniotic fluid and IL1β in placental tissue of MgBL (P<0.001) (Fig. 1) . Neither maternal nor fetal plasma showed differences in cytokine levels.
Maternal oral magnesium supplementation reduced the incidence of BL-induced IUGR by 64% and modulated cytokine expression in amniotic fluid and placentas obtained from live IUGR fetuses in absence of maternal systemic inflammation. Supported by Oxenhorn Family.