Hydrogen Gas Protects Liver from Alcohol Damage in Mouse Study
- Authors
- Luyao Xu, Wenhai Guo, Jiaying Dai, Ya Cheng, Yun Chen, Wei Liu, Jiean Xu, Wen Su, Xiaodong Zhang, Changjun Wang, Yang Hongzhi, Jinwen Xu, Yaxing Zhang
- Journal
- International Immunopharmacology
- Year
- 2023
- DOI
- 10.1016/j.intimp.2023.111399
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Alcoholic Liver Disease
- Body System
- Hepatic
TL;DR
Injecting hydrogen gas into the abdomen of mice reduces liver damage caused by heavy alcohol use by decreasing inflammation and oxidative stress.
Key Finding
Hydrogen gas injected into mice reduced acute alcohol-induced liver damage by lowering oxidative stress, suppressing inflammatory immune signaling, and blocking multiple cell death pathways in a dose-dependent manner.
Summary
Researchers gave mice hydrogen gas through injection and then exposed them to alcohol to see if hydrogen could protect their livers. They found that hydrogen gas reduced liver damage by decreasing harmful molecules called free radicals (unstable atoms that damage cells), reducing inflammation, and preventing a type of cell death called pyroptosis. The protective effects increased with higher doses of hydrogen.
Practical Takeaway
This is an early-stage animal study showing hydrogen gas may help protect liver cells from alcohol damage through multiple biological mechanisms. However, these results are from mice receiving direct gas injections—not from drinking hydrogen water—so it's unclear whether similar benefits would occur in humans or with other hydrogen delivery methods. More research is needed before any conclusions can be drawn for human health.
Abstract
Alcoholic liver disease (ALD), which is induced by chronic heavy alcohol consumption, accompanies complicated pathological mechanisms, including oxidative stress, inflammation, cell death, epigenetic changes and acetaldehyde-mediated toxicity. Hydrogen (H2) is the lightest gas with multiple biological effects such as high selective anti-oxidation, anti-inflammation and anti-apoptosis. However, the dose effects and innate immune mechanisms of intraperitoneal injection of H2 on ALD are limited. Here, we used acute ethanol-induced hepatotoxicity mice models to estimate the actions of intraperitoneal injection of H2 on ALD. The effects of H2 on acute ethanol-induced liver damage were examined by hepatic oil red O staining, quantitative PCR (qPCR) for lipid metabolic genes, hepatic triglyceride (TG) and serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Hepatic mitochondrial superoxide (MitoSOX), 3-nitrotyrosine (3-NT), malondialdehyde (MDA), and glutathione (GSH) levels were examined to evaluate oxidative stress. Immunoblot, and immunofluorescence staining were used to further confirm the innate immune molecular targets of H2. Our results showed that intraperitoneal injection of H2 improved acute ethanol-induced liver injury in mice in a dose dependent manner, as indicated by decreasing serum ALT and AST levels, hepatic TG levels, and increasing lipid export genes (Mttp and Apob) mRNA levels and reducing fatty acid uptake gene (CD36) mRNA levels. Mechanistically, H2 inhibited hepatic oxidative stress as indicated by reducing reactive oxygen species (ROS), 3-NT, and MDA levels in the liver, while increasing hepatic GSH levels; inhibited the overactived TLR4/9-NF-κB-TNF-α/IL-1β/IL-18 innate immune signaling; suppressed the canonical Caspase-1-GSDMD pyroptosis signaling, and the non-canonical pyroptosis signaling, such as Caspase-11-GSDMD, Caspase-8-GSDMD and Caspase-3-GSDME signaling. Therefore, our study highlights that intraperitoneal injection of H2 may represent a novel therapeutic and safe strategy for ALD via modulating oxidative stress, innate immunity and pyroptosis.