Hydrogen Protects Liver Bile Duct Cells from Surgical Damage
- Authors
- Jianhua Yu, Weiguang Zhang, Rongguo Zhang, Guixing Jiang, Haijun Tang, Xinxian Ruan, Peitu Ren, Baochun Lu
- Journal
- Toxicology Letters
- Year
- 2015
- DOI
- 10.1016/j.toxlet.2015.08.010
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Liver Surgery Complications
- Body System
- Hepatobiliary
TL;DR
Molecular hydrogen (H2) can protect liver cells from damage caused by oxygen deprivation and subsequent reoxygenation by activating a protective protein.
Key Finding
Molecular hydrogen protected liver cholangiocytes from oxygen-deprivation injury by activating the Nrf2 antioxidant defense pathway, and this protection was lost when Nrf2 was disabled.
Summary
Researchers tested whether molecular hydrogen (H2) could protect liver cells called cholangiocytes from damage caused by temporary loss of oxygen followed by oxygen restoration—a type of injury that can occur during liver surgery. Using human liver cells in the lab and rat models, they found that hydrogen reduced cell death and activated a protective protein pathway (Nrf2) that helps cells defend against oxidative stress (cellular damage from harmful molecules).
Practical Takeaway
This early laboratory and animal research suggests hydrogen water may have potential to protect liver cells during surgical stress, but the findings are limited to cell cultures and rat models. Human studies would be needed to determine whether hydrogen water could provide similar benefits in actual surgical patients or whether it could be used preventively.
Abstract
Hypoxia/reoxygenation (H/R) injury of cholangiocytes causes serious biliary complications during hepatobiliary surgeries. Molecular hydrogen (H2) has been shown to be effective in protecting various cells and organs against oxidative stress injury. Human liver cholangiocytes were used to determine the potential protective effects of hydrogen against cholangiocyte H/R injury and explore the underlying mechanisms. We found that H2 ameliorated H/R-induced cholangiocytes apoptosis. Our study revealed that H2 activated NF-E2-related factor 2 (Nrf2) and downstream cytoprotective protein expression. However, the protective function of H2 was abolished when Nrf2 was silenced. Apoptosis in cholangiocytes isolated from a rat model of liver ischemia/reperfusion injury indicated that H2 significantly attenuates ischemia/reperfusion cholangiocyte injury in vivo. In conclusion, our study shows that H2 protects intrahepatic cholangiocytes from hypoxia/reoxygenation-induced apoptosis in vitro or in vivo, and this phenomenon may depend on activating Nrf2 expression.