Hydrogen Water May Help Prevent Preterm Birth in Animal Study

Authors
Journal
Biomedical Reports
Year
DOI
10.3892/br.2018.1082
Study Type
Mouse
Outcome
Positive
Peer Reviewed
Yes
Country
Japan
Health Condition
Preterm Labor
Body System
Reproductive

TL;DR

Drinking hydrogen-enriched water before an inflammatory trigger can delay preterm labor in mice by reducing inflammation in the womb.

Key Finding

In pregnant mice, hydrogen water administration delayed preterm labor onset by approximately 15 hours and reduced multiple inflammatory markers in the uterus compared to untreated mice.

Summary

Researchers gave pregnant mice hydrogen-enriched water to see if it could prevent early labor caused by inflammation. Mice that received hydrogen water before being exposed to an inflammatory trigger delivered their babies about 15 hours later than mice without hydrogen water treatment. The hydrogen water also reduced inflammatory markers (chemical signals of inflammation) in the uterus and increased progesterone levels, a hormone important for maintaining pregnancy.

Practical Takeaway

This is an early-stage animal study suggesting hydrogen water may help suppress inflammation related to preterm labor, but it cannot yet inform human treatment decisions. Research in pregnant women would be needed before any clinical recommendations could be made, and anyone concerned about preterm labor should consult their healthcare provider about proven prevention strategies.

Abstract

Intrauterine inflammation causes preterm birth and is associated with complications in preterm neonates. Thus, strategies aimed at suppressing inflammation are expected to be effective for reducing the risk of preterm birth and associated complications. Our previous studies demonstrated that molecular hydrogen (H2), an anti-inflammatory agent, prevented inflammation-induced impairment in foetal brain and lung tissues in lipopolysaccharide (LPS)-induced rodent models. However, it remains unclear whether H2 is capable of inhibiting preterm labour. The aim of the current study was therefore to investigate the effect of H2 on inflammation-induced preterm labour. Pregnant ICR (CD-1) mice were divided into three groups: Control, LPS and H2 water (HW) + LPS. In the control and LPS groups, vehicle and LPS, respectively, were intraperitoneally injected on embryonic day 15.5. In the HW + LPS group, HW was administered 24 h prior to LPS injection. The time from LPS administration to parturition was compared between the LPS and HW + LPS groups. Maternal uterus was collected 6 h after LPS injection and the transcript levels of pro-inflammatory cytokines, contractile-associated proteins (CAPs), matrix metalloproteinase-3 (Mmp3) and endothelin-1 (Et1) were assessed by reverse transcription-quantitative polymerase chain reaction. The protein levels of cyclooxygenase-2 (Cox2) were also evaluated by immunohistochemistry. The time from LPS administration to parturition in the HW + LPS group was significantly increased compared with that in the LPS group (33.5±3.4 vs. 18.3±8.8 h, respectively, P=0.020). H2 administration also resulted in significantly higher progesterone levels compared with LPS treatment alone (P=0.002). The transcript levels of pro-inflammatory cytokines, CAPs, Mmp3 and Et1 in the uteri of the LPS group were significantly higher than those in the control group (all P<0.05). In turn, all these levels with the exception of interleukin-8 and Mmp3 were significantly lower in the HW + LPS group compared with those in the LPS group (all P<0.05). The protein levels of Cox2 in the LPS group were also significantly increased compared with those in the control (P<0.001) and HW + LPS (P=0.003) groups. These results suggest that inflammation-induced changes in the uterus may be ameliorated through maternal H2 administration. Preventive H2 administration may therefore represent an effective strategy for the suppression of inflammation during preterm labour.