Hydrogen Water Reduces Pancreas Inflammation in Mice Study
- Authors
- Jian-Dong Ren, Jie Ma, Jun Hou, Wen-Jin Xiao, Wei-Hua Jin, Juan Wu, Kai-Hua Fan
- Journal
- Mediators of Inflammation
- Year
- 2014
- DOI
- 10.1155/2014/930894
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Acute Pancreatitis
- Body System
- Digestive System
TL;DR
A study found that hydrogen-rich saline can reduce inflammation and tissue damage in mice with acute pancreatitis by blocking a specific inflammatory protein complex.
Key Finding
Hydrogen-rich saline substantially inhibited NLRP3 inflammasome activation in mice with acute pancreatitis, reducing oxidative stress and inflammatory markers while preserving pancreatic tissue.
Summary
This mouse study investigated whether hydrogen-rich saline (a salt solution containing dissolved hydrogen) could help treat acute pancreatitis (sudden inflammation of the pancreas). Researchers induced pancreatitis in mice and treated some with hydrogen-rich saline. They found that the treatment reduced harmful molecules called reactive oxygen species, decreased inflammation, and protected pancreatic tissue by blocking a specific inflammatory pathway called NLRP3.
Practical Takeaway
This early animal evidence suggests hydrogen-rich saline may help reduce inflammation in acute pancreatitis by targeting a specific inflammatory pathway. However, this is a mouse study only, and human trials would be needed to determine if these results apply to people with pancreatitis.
Abstract
Increasing evidence has demonstrated that reactive oxygen species (ROS) induces oxidative stress and plays a crucial role in the pathogenesis of acute pancreatitis (AP). Hydrogen-rich saline (HRS), a well-known ROS scavenger, has been shown to possess therapeutic benefit on AP in many animal experiments. Recent findings have indicated that the NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome, an intracellular multiprotein complex required for the maturation of interleukin- (IL-) 1β, may probably be a potential target of HRS in the treatment of AP. Therefore, in this study, we evaluated the activation of NLRP3 inflammasome and meanwhile assessed the degree of oxidative stress and inflammatory cascades, as well as the histological alterations in mice suffering from cerulein-induced AP after the treatment of HRS. The results showed that the activation of NLRP3 inflammasome in AP mice was substantially inhibited following the administration of HRS, which was paralleled with the decreased NF-κB activity and cytokines production, attenuated oxidative stress and the amelioration of pancreatic tissue damage. In conclusion, our study has, for the first time, revealed that inhibition of the activation of NLRP3 inflammasome probably contributed to the therapeutic potential of HRS in AP.