Hydrogen Therapy Helps Liver Recovery from Bile Duct Blockage
- Authors
- Zhiyang Zhu, Jianhua Yu, Weiguo Lin, Haijun Tang, Weiguang Zhang, Baochun Lu
- Journal
- Molecular Medicine Reports
- Year
- 2019
- DOI
- 10.3892/mmr.2019.10179
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Acute Obstructive Cholangitis
- Body System
- Hepatobiliary
TL;DR
Hydrogen gas treatment helps repair liver damage caused by acute obstructive cholangitis (AOC) by fixing the connections between liver cells.
Key Finding
Molecular hydrogen administration reversed liver damage caused by acute obstructive cholangitis in rats by restoring damaged junction proteins between liver cells and reducing inflammatory and oxidative damage.
Summary
This study used rats with a type of liver infection caused by bile duct blockage to test whether molecular hydrogen (H2) could help repair liver damage. Researchers found that the infection damaged important protein structures (called gap junctions and tight junctions) that help liver cells communicate and stay connected. When hydrogen was given to the rats after the bile duct was drained, it helped restore these damaged protein structures and reduced inflammation and oxidative stress (cellular damage from harmful molecules), which accelerated liver recovery.
Practical Takeaway
This is an early-stage animal study showing hydrogen may help protect liver function during severe bile duct infections. However, this research was only conducted in rats, and the study duration and sample size were not reported, so it's too preliminary to draw conclusions about effectiveness in humans. More research, including human trials, would be needed before hydrogen could be considered a therapeutic option for this condition.
Abstract
Gap junctions (GJs) and tight junctions (TJs) are essential to maintain the function of hepatocytes. Changes in biliary tract pressure and the effect of lipopolysaccharide (LPS) may lead to acute obstructive cholangitis (AOC) and cause liver injury via GJ and TJ dysfunction. Hydrogen has been confirmed to have a protective role in various organs during pathological conditions and inflammation. The present study investigated the function of junction proteins and the potential application of H2 in AOC‑induced liver injury. An AOC rat model was established by LPS injection through a bile duct catheter, while the distal bile duct was closed. The catheter sealing caps were removed and bile was allowed to flow out from the catheters at 12 h after LPS infusion. The potential application of H2 was studied in the AOC rat model with biliary drainage. It was observed that AOC induced the disruption of junction proteins of both GJs and TJs. H2 administration reversed AOC‑induced disruption of GJs and TJs after biliary drainage. The mechanism of this phenomenon suggests that H2 may have effectively attenuated AOC‑induced inflammatory and oxidative damage, and decreased matrix metalloproteinase activity. H2 may accelerate the reversal of AOC‑induced liver dysfunction, and this phenomenon may depend on reversing the inhibition of GJs and TJs.