Hydrogen Gas Reduces Pancreatic Inflammation Through Key Cell Pathways
- Authors
- Bing Han, Haoxin Zhou, Guang Jia, Yongwei Wang, Zengfu Song, Gang Wang, Shangha Pan, Xuewei Bai, Jiachen Lv, Bei Sun
- Journal
- The FEBS Journal
- Year
- 2016
- DOI
- 10.1111/febs.13629
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Acute Pancreatitis
- Body System
- Digestive System
TL;DR
Hydrogen gas treatment can help reduce inflammation and protect against pancreas damage by affecting certain cell signaling pathways and proteins.
Key Finding
Molecular hydrogen reduces pancreatic inflammation during acute pancreatitis by blocking specific cellular signaling pathways (MAPK and NF-κB) and increasing a protective protein (Hsc70).
Summary
This study investigated how molecular hydrogen protects the pancreas during acute pancreatitis (sudden pancreatic inflammation). Researchers used laboratory cell cultures and animal models to identify which proteins and cellular pathways hydrogen affects. They found that hydrogen reduces inflammation by blocking certain signaling pathways (called MAPK and NF-κB) that trigger inflammatory molecules, while also increasing production of a protective protein called Hsc70.
Practical Takeaway
This laboratory and animal study provides early evidence for how hydrogen might work against pancreatic inflammation at the cellular level. However, these findings are from cell cultures and animal models, not human studies, so it remains unclear whether these protective effects would occur in people with acute pancreatitis. Further human research would be needed to determine if hydrogen therapy could be a practical treatment option.
Abstract
Molecular hydrogen (H2) has been proven to be an effective agent that can cure multiple organ diseases by reducing oxidative stress. Although the protective effect of hydrogen on acute pancreatitis (AP) has been confirmed, its molecular mechanism is still unclear. In this article, we aimed to investigate the changes in pancreatic cell protein expression associated with the protective effect of H2 against AP and attempted to uncover the molecular mechanism underlying this process. A proteomic analysis identified 73 differentially expressed proteins and generated the protein–protein interaction networks of these proteins. The results triggered our interest in mitogen‐activated protein kinase (MAPK) and heat shock cognate 71 kDa protein (Hsc70). The subsequent in vitro experiments showed that H2 treatment inhibited the phosphorylation of extracellular signal‐regulated kinase (ERK), c‐jun N‐terminal kinase (JNK), and p38 MAPK, and activated NF‐κB and the expression of tumor necrosis factor α and interleukin‐1β, while simultaneously preventing the translocation of phospho‐ERK, phospho‐JNK, and phospho‐p38 from the cytoplasm to the nucleus. Furthermore, Hsc70 expression was upregulated by H2 administration. The animal experimental results were consistent with those of the in vitro experiments. In conclusion, H2 treatment can ameliorate the inflammatory response and reduce the expression of inflammatory mediators during the early phase of AP by inhibiting the MAPK pathways and increasing Hsc70 expression.