Hydrogen Water Protects Liver from Pancreatic Damage in Rats
- Authors
- Qiao Shi, Chen Chen, Wen-hong Deng, Peng Wang, Teng Zuo, Liang Zhao, Jia Yu, Kai-liang Zhao, Fang-chao Mei, Chen Li, Gui-rong Wang, Wei-xing Wang
- Journal
- Pancreas
- Year
- 2016
- DOI
- 10.1097/MPA.0000000000000678
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Acute Necrotizing Pancreatitis
- Body System
- Hepatic
TL;DR
Hydrogen-rich saline may help protect the liver from damage during severe pancreatitis by reducing inflammation and cell death.
Key Finding
Hydrogen-rich saline reduced liver damage in rats with acute necrotizing pancreatitis by decreasing oxidative stress and blocking inflammatory cell-death pathways.
Summary
This study tested whether hydrogen-rich saline (salt water containing dissolved hydrogen) could protect the liver from damage during acute necrotizing pancreatitis (a severe pancreas inflammation) in rats. Researchers induced pancreatitis in rats and gave some of them hydrogen-rich saline while monitoring liver function and cellular damage markers. The treatment reduced liver damage, decreased harmful molecules called free radicals, and blocked inflammatory pathways that trigger cell death.
Practical Takeaway
This is early-stage research in animals only, so it cannot yet inform human health decisions. The findings suggest hydrogen-rich saline may have protective effects against pancreatitis-related liver injury, but human studies would be needed to determine if this applies to people and whether it could be a useful treatment.
Abstract
Objectives: The objective of this study was to study the role of hydrogen-rich saline (HRS) on acute hepatic injury (AHI) in acute necrotizing pancreatitis (ANP). Methods: Rats were used for this study and an ANP model was induced by injecting 5% sodium taurocholate into the biliary-pancreatic duct. Experiments were performed in 3 groups: sham, ANP, and ANP + HRS (HRS). Animals were killed at 3, 12, and 24 hours after operation, and then blood and tissue samples were harvested. Various physiological, histological, and cellular and molecular parameters were analyzed. Results: Analyses of serum, lipase, alanine transaminase, and aspartate aminotransferase indicated that ANP-induced AHI model was established successfully and HRS attenuated hepatic dysfunction. Hepatic superoxide dismutase and malondialdehyde levels showed HRS against oxidative stress. Cellular and molecular analyses including p-p38, p-JNK, p-ERK, and caspase-3, caspase-9, NF-κB, and TNF-α in hepatic tissues revealed that HRS attenuated ANP-induced AHI by inhibiting apoptosis and phosphorylation of JNK and p38, as well as NF-κB activation. Conclusions: Hydrogen-rich saline plays a protective role in ANP-induced AHI through inhibiting inflammation and apoptosis, involving JNK and p38 MAPK-dependent reactive oxygen species.