Hydrogen Gas Protects Against Severe Pancreas Inflammation in Rats

Authors
Journal
PLoS One
Year
DOI
10.1371/journal.pone.0154483
Study Type
Rat
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Acute Pancreatitis
Body System
Digestive System

TL;DR

Breathing in hydrogen gas can reduce inflammation and damage in the pancreas during acute pancreatitis.

Key Finding

Hydrogen gas reduced inflammation and oxidative stress markers in both laboratory pancreatic cells and in rats with acute pancreatitis, and was associated with less pancreatic tissue damage.

Summary

Acute pancreatitis is a serious inflammatory disease where the pancreas becomes damaged and inflamed, often leading to widespread inflammation throughout the body. This study tested whether hydrogen gas could protect against pancreatic damage by reducing inflammation and oxidative stress (cellular damage from harmful molecules). Researchers tested hydrogen gas in both laboratory cell cultures and in rats with induced pancreatitis, and found that hydrogen gas reduced markers of inflammation, oxidative stress, and pancreatic tissue damage in both settings.

Practical Takeaway

This early-stage animal study suggests hydrogen gas may have protective effects against acute pancreatitis, but the findings are limited to laboratory and rat models and have not been tested in humans. Much more research would be needed before any conclusions could be drawn about hydrogen's potential use in treating pancreatitis in people.

Abstract

Acute pancreatitis (AP) is an inflammatory disease mediated by damage to acinar cells and pancreatic inflammation. In patients with AP, subsequent systemic inflammatory responses and multiple organs dysfunction commonly occur. Interactions between cytokines and oxidative stress greatly contribute to the amplification of uncontrolled inflammatory responses. Molecular hydrogen (H2) is a potent free radical scavenger that not only ameliorates oxidative stress but also lowers cytokine levels. The aim of the present study was to investigate the protective effects of H2 gas on AP both in vitro and in vivo. For the in vitro assessment, AR42J cells were treated with cerulein and then incubated in H2-rich or normal medium for 24 h, and for the in vivo experiment, AP was induced through a retrograde infusion of 5% sodium taurocholate into the pancreatobiliary duct (0.1 mL/100 g body weight). Wistar rats were treated with inhaled air or 2% H2 gas and sacrificed 12 h following the induction of pancreatitis. Specimens were collected and processed to measure the amylase and lipase activity levels; the myeloperoxidase activity and production levels; the cytokine mRNA expression levels; the 8-hydroxydeoxyguanosine, malondialdehyde, and glutathione levels; and the cell survival rate. Histological examinations and immunohistochemical analyses were then conducted. The results revealed significant reductions in inflammation and oxidative stress both in vitro and in vivo. Furthermore, the beneficial effects of H2 gas were associated with reductions in AR42J cell and pancreatic tissue damage. In conclusion, our results suggest that H2 gas is capable of ameliorating damage to the pancreas and AR42J cells and that H2 exerts protective effects both in vitro and in vivo on subjects with AP. Thus, the results obtained indicate that this gas may represent a novel therapy agent in the management of AP.