Hydrogen Water Protects Unborn Babies' Brains from Inflammation

Authors
Journal
Journal of Clinical Biochemistry and Nutrition
Year
DOI
10.3164/jcbn.15-90
Study Type
Mouse
Outcome
Positive
Peer Reviewed
Yes
Country
Japan
Health Condition
Fetal Brain Injury
Body System
Nervous System

TL;DR

Giving pregnant mice hydrogen-rich water before inducing inflammation reduced brain damage in their unborn babies.

Key Finding

In pregnant mice, hydrogen water administration reduced fetal brain damage from inflammation-triggering bacterial toxin by decreasing cell death, oxidative damage, and inflammatory markers.

Summary

Researchers studied whether hydrogen water could protect fetal mouse brains from injury caused by a bacterial toxin (lipopolysaccharide) that triggers inflammation. Pregnant mice received hydrogen water for 24 hours before being exposed to the toxin. The study found that hydrogen water reduced three markers of brain damage in the fetuses: cell death, oxidative stress (cellular damage from unstable molecules), and inflammatory signaling molecules.

Practical Takeaway

This is an early-stage animal study in mice, not humans, so its relevance to human pregnancy is unknown. While the results suggest hydrogen water may have protective effects against inflammation-related fetal brain injury, much more research—including human studies—would be needed before any clinical recommendations could be made. Pregnant individuals should consult their healthcare provider before using any new interventions.

Abstract

Fetal brain injury is often related to prenatal inflammation; however, there is a lack of effective therapy. Recently, molecular hydrogen (H2), a specific antioxidant to hydroxyl radical and peroxynitrite, has been reported to have anti-inflammatory properties. The aim of this study was to investigate whether maternal H2 administration could protect the fetal brain against inflammation. Pregnant C3H/HeN mice received an intraperitoneal injection of lipopolysaccharide (LPS) on gestational day 15.5 and were provided with H2 water for 24 h prior to LPS injection. Pup brain samples were collected on gestational day 16.5, and the levels of apoptosis and oxidative damage were evaluated using immunohistochemistry. Interleukin-6 (IL-6) levels were examined using real-time PCR. The levels of apoptosis and oxidative damage, as well as the levels of IL-6 mRNA, increased significantly when the mother was injected with LPS than that in the control group. However, these levels were significantly reduced when H2 was administered prior to the LPS-injection. Our results suggest that LPS-induced apoptosis, oxidative damage and inflammation in the fetal brain were ameliorated by maternal H2 administration. Antenatal H2 administration might protect the premature brain against maternal inflammation.