Hydrogen Water Protects Fatty Liver from Surgery Damage in Mice
- Authors
- Shaowei Li, Masayuki Fujino, Naotsugu Ichimaru, Ryosuke Kurokawa, Shinichi Hirano, Lisha Mou, Shiro Takahara, Terumi Takahara, Xiao-Kang Li
- Journal
- Scientific Reports
- Year
- 2018
- DOI
- 10.1038/s41598-018-32411-4
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Fatty Liver Disease
- Body System
- Hepatic
TL;DR
Hydrogen-infused saline can reduce liver damage caused by blood flow disruptions in mice with fatty liver disease.
Key Finding
Hydrogen saline treatment significantly reduced liver damage markers and cell death in fatty livers undergoing ischemia-reperfusion injury, while increasing protective proteins HO-1 and Sirt1.
Summary
This study tested whether hydrogen gas dissolved in saline could protect fatty livers from damage during ischemia-reperfusion injury—a type of damage that occurs when blood flow to the liver is cut off and then restored, common during liver transplantation. Using mice with fatty livers, researchers gave hydrogen-containing saline during the injury process and found that hydrogen treatment reduced liver cell death, decreased inflammation, and activated protective proteins in the liver.
Practical Takeaway
This is early-stage research in mice only, not humans. While the results suggest hydrogen may have potential to protect liver tissue during transplantation procedures, much more research—including human studies—would be needed before any clinical application. The findings cannot be applied to drinking hydrogen water or other consumer uses at this time.
Abstract
Fatty liver has lower tolerance against ischemia-reperfusion (I/R) injury in liver operations, including liver transplantation. Seeking to ameliorate liver injury following I/R in fatty liver, we examined the protective effect of hydrogen (H2) saline on I/R liver injury in a methionine and choline-deficient plus high fat (MCDHF) diet-induced fatty liver mouse model. Saline containing 7 ppm H2 was administrated during the process of I/R. Livers were obtained and analyzed. Primary hepatocytes and Kupffer cells (KCs) were obtained from fatty liver and subjected to hypoxia/reoxygenation. Apoptosis-related proteins and components of the signaling pathway were analyzed after treatment with hydrogen gas. The MCDHF I/R group showed higher levels of AST and ALT in serum, TUNEL-positive apoptotic cells, F4/80 immunopositive cells, mRNA levels of inflammatory cytokines, constituents of the signaling pathway, pro-apoptotic molecules in liver, and KCs and/or primary hepatocytes, compared to the control group. In contrast, H2 treatment significantly suppressed the signs of I/R injury in fatty liver. Moreover, the expression of Bcl-2, HO-1, and Sirt1 in liver, KCs, and hepatocytes by hydrogen gas were increased, whereas caspase activation, Bax, and acetylation of p53 were suppressed by hydrogen gas. These results demonstrated that H2 treatment ameliorated I/R liver injury in a fatty liver model by reducing hepatocyte apoptosis, inhibiting macrophage activation and inflammatory cytokines, and inducing HO-1 and Sirt1 expression. Taken togather, treatment with H2 saline may have a protective effect and safe therapeutic activity during I/R events, such as in liver transplantation with fatty liver.