Hydrogen Water Protects Liver from Chronic Inflammation in Rats
- Authors
- Luyao Zhang, Hanyu Wang, Yingxuan Mai, Qi He, Tao Liu, Na Zhang, Jiantao Zhang
- Journal
- Antioxidants
- Year
- 2026
- DOI
- 10.3390/antiox15020260
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Chronic Liver Disease
- Body System
- Hepatic
TL;DR
Long-term hydrogen-rich water consumption reduced chronic liver inflammation and apoptosis in a rat model of LPS-induced hepatic injury.
Key Finding
Long-term hydrogen-rich water consumption significantly reduced inflammatory cell infiltration, suppressed pro-inflammatory factors, and prevented liver cell death in rats with chronic liver inflammation.
Summary
Researchers gave rats hydrogen-rich water for 8 months, then induced chronic liver inflammation in them and continued the treatment. The hydrogen-rich water reduced inflammation in liver tissue, lowered harmful inflammatory molecules, and prevented liver cells from dying through multiple cellular pathways. This suggests hydrogen-rich water may help protect the liver from long-term inflammatory damage.
Practical Takeaway
This rat study suggests hydrogen-rich water may have protective effects against chronic liver inflammation, but these results cannot be directly applied to humans yet. Further research in human subjects would be needed to determine if similar benefits occur in people.
Abstract
(1) Background: Chronic inflammation is considered an important pathological basis underlying the development and progression of multiple metabolic liver diseases; although hydrogen-rich water (HRW) has shown beneficial effects in acute inflammation, its long-term impact on chronic hepatic inflammation remains unclear. (2) Methods: Sprague-Dawley rats were pretreated with HRW for 8 months, after which a lipopolysaccharide (LPS)-induced rat model of chronic hepatic inflammation was established, with continuous HRW administration throughout the experimental period. (3) Results: Long-term HRW consumption significantly reduced LPS-induced inflammatory cell infiltration in liver tissue, suppressed the abnormal elevation of pro-inflammatory factors, and maintained relatively stable expression levels of anti-inflammatory factors. In addition, HRW attenuated pro-apoptotic signaling associated with the death receptor pathway, mitochondrial pathway, and endoplasmic reticulum stress (including Bax, Cyt c, Caspase-3, Caspase-8, Caspase-9, Caspase-12, CHOP, and GRP78), while preserving the expression of the anti-apoptotic protein Bcl-2, thereby partially preventing the tendency toward hepatocyte apoptosis induced by chronic inflammation. (4) Conclusions: Long-term consumption of HRW may delay the onset and progression of chronic inflammation-related liver injury by alleviating inflammatory responses, oxidative stress, mitochondrial dysfunction, and apoptotic activity, thus exerting a preventive protective effect on the liver.