Hydrogen Water Protects Liver from Surgery-Related Damage in Rats

Authors
Journal
Digestive Diseases and Sciences
Year
DOI
10.1007/s10620-017-4811-8
Study Type
Rat
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Hepatic Ischemia-Reperfusion Injury
Body System
Hepatic

TL;DR

Hydrogen-rich saline (HS) helps reduce liver damage and cell death caused by temporary loss of blood supply followed by restoration (ischemia-reperfusion injury).

Key Finding

Hydrogen-rich saline significantly reduced liver damage markers and cell death in rats experiencing ischemia-reperfusion injury, with improvements linked to reduced stress in the endoplasmic reticulum (a cellular structure involved in protein production).

Summary

This study tested whether hydrogen-rich saline (salt water containing dissolved hydrogen gas) could protect rat livers from damage caused by temporarily cutting off blood flow and then restoring it—a type of injury that can occur during liver surgery. Researchers compared livers treated with hydrogen-rich saline to those treated with regular saline after different periods of blood flow interruption. Livers treated with hydrogen-rich saline showed better function, less oxidative damage (a type of cellular injury), and fewer dying cells compared to the control group.

Practical Takeaway

While these results are promising, this is an animal study in rats, so it's unclear whether the same protective effects would occur in humans. Early evidence suggests hydrogen-rich saline may help protect liver tissue during surgical procedures involving blood flow interruption, but human clinical trials would be needed before any medical applications could be recommended.

Abstract

Objective: To evaluate the effect of hydrogen-rich saline (HS) on hepatic ischemia-reperfusion (I/R) injury. Methods: Forty rats were randomly allocated into five groups: one sham group (control group), one group treated with 20 min of ischemia and normal saline (NS; I/R1 + NS group), one group treated with 20 min of ischemia and HS (I/R1 + HS group), one group treated with 60 min of ischemia and NS (I/R2 + NS group), and one group treated with 60 min of ischemia and HS (I/R2 + HS group). After reperfusion for 6 h, hepatic function, oxidative stress, pathological changes, and apoptosis of hepatic cells were evaluated. Furthermore, the expression levels of endoplasmic reticulum (ER) stress-associated proteins were identified. Results: Serum ALT and AST levels and tissue MDA content in the I/R + HS groups were significantly lower than those in the I/R + NS groups. Pathological changes were also significantly ameliorated in the HS groups compared with those in the NS groups. Moreover, HS appeared to significantly attenuate hepatic I/R-induced ER stress responses, as indicated by the decreased expression of C/EBP homologous protein, protein-kinase-RNA-like ER kinase, and inositol-requiring protein-1α, as well as the increased expression of GRP78 proteins. Finally, the levels of apoptotic markers such as caspase-3 and TUNEL-positive cells were significantly lower in the HS groups than in the NS control groups, whereas the level of Bcl2 protein increased in the HS groups. Conclusion: The protective effect of HS can be attributed to ER stress and apoptosis inhibition.