Systemic administration of betamethasone delays endotoxin-induced preterm labor in the murine model

Abstract

Objective: The purpose of this study was to determine whether the administration of betamethasone decreases the endotoxin-induced preterm parturition rate and inhibits the risk of cytokines in the murine model. Study design: Endotoxin was administered intraperitoneally at gestational day 15 (75% of gestation). In phase I, the duration of gestation was measured in 36 gravid C3H/HeOu mice that were equally divided into four treatment groups: control, endotoxin only, and two different dose regimens of betamethasone followed by endotoxin. In phase II, maternal serum and amniotic fluid concentrations of cytokines (interleukin-1α, tumor necrosis factor-α, and interleukin-6) were measured at 4 hours after endotoxin injection in 44 gravid mice divided equally in the four treatment groups. Results: The group that was exposed only to endotoxin was delivered at a significantly earlier gestational age compared with the control group (16.2 ± 0.4 days vs 19.6 ± 0.2 days; P < .01). The two groups that were pretreated with betamethasone before the endotoxin were delivered at gestational ages similar to the control group. There was a marked increase of tumor necrosis factor-α and interleukin-6 levels in amniotic fluid of mice that were treated with endotoxin only compared with the control group (P < .001). No difference in cytokine levels was found in those mice that were premedicated with betamethasone compared with the control group. Conclusion: Antenatal administration of betamethasone to mice delayed preterm parturition that was induced by endotoxin. Elevations of amniotic fluid cytokine concentrations that were observed with endotoxin were not observed with pretreatment with betamethasone. (Am J Obstet Gynecol 2003;188:439-43.)