Hydrogen Gas Protects Liver from Chemical Damage in Rat Study
- Authors
- Jianwei Wang, Quancheng Cheng, Jinyu Fang, Huiru Ding, Huaicun Liu, Xuan Fang, Chunhua Chen, Weiguang Zhang
- Journal
- Antioxidants
- Year
- 2021
- DOI
- 10.3390/antiox10121933
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Chronic Liver Injury
- Body System
- Hepatic
TL;DR
Breathing in hydrogen gas reduced liver damage and fat buildup in rats with early signs of liver injury, possibly by increasing levels of a protective protein in the liver.
Key Finding
Hydrogen gas inhalation reduced fat accumulation in rat liver cells damaged by CCl4 and increased levels of a protective protein (UCP2) in liver tissue.
Summary
Researchers gave rats a toxic chemical (CCl4) that damages the liver, then exposed some rats to hydrogen gas to see if it would help. They found that hydrogen gas reduced fat buildup in liver cells and increased a protective protein called UCP2, suggesting hydrogen may protect liver cells by reducing harmful molecules called free radicals.
Practical Takeaway
This is an early-stage animal study showing hydrogen gas may help protect liver cells from chemical damage, but it was only tested in rats. Much more research, including human studies, would be needed before any conclusions could be drawn about hydrogen water's effects on human liver health.
Abstract
As a small-molecule reductant substance, hydrogen gas has an obvious antioxidant function. It can selectively neutralize hydroxyl radicals (•OH) and peroxynitrite (ONOO•) in cells, reducing oxidative stress damage. The purpose of this study was to investigate the effect of hydrogen gas (3%) on early chronic liver injury (CLI) induced by CCl4 and to preliminarily explore the protective mechanism of hydrogen gas on hepatocytes by observing the expression of uncoupling protein 2 (UCP2) in liver tissue. Here, 32 rats were divided into four groups: the control group, CCl4 group, H2 (hydrogen gas) group, and CCl4 + H2 group. The effect of hydrogen gas on early CLI was observed by serological tests, ELISA, hematoxylin and eosin staining, and oil red O staining. Immunohistochemical staining and Western blotting were used to observe the expression of UCP2 in liver tissues. We found that CCl4 can induce significant steatosis in hepatocytes. When the hydrogen gas was inhaled, hepatocyte steatosis was reduced, and the UCP2 expression level in liver tissue was increased. These results suggest that hydrogen gas might upregulate UCP2 expression levels, reduce the generation of intracellular oxygen free radicals, affect lipid metabolism in liver cells, and play a protective role in liver cells.