Can hydrogen gas help prevent brain damage during sepsis?

This study suggests yes - hydrogen gas inhalation significantly protected brain function in mice with sepsis. The treatment prevented cognitive decline and preserved memory abilities by blocking harmful protein changes in neurons.

How does hydrogen therapy protect the brain during infections?

Hydrogen gas appears to work by preventing tau proteins in brain neurons from becoming over-phosphorylated, which normally damages cells during inflammation. It also reduces neuroinflammation and preserves the structure of neurons.

What cognitive problems does sepsis cause?

Sepsis can cause sepsis-associated encephalopathy, leading to memory problems, difficulty learning new information, and general cognitive decline. These issues can persist long after the infection is treated.

How was hydrogen gas administered in this study?

Mice breathed 2% hydrogen gas for 60 minutes at two time points - 1 hour and 6 hours after sepsis was induced. This inhalation method delivered the therapeutic gas directly to the bloodstream and brain.

Is hydrogen therapy safe for treating brain complications?

Hydrogen gas has an excellent safety profile and is already used clinically in some countries. This study showed no adverse effects, and hydrogen therapy actually improved survival rates in septic mice.

Hydrogen Gas Protects Brain Function During Life-Threatening Infections

Authors: Bo Qi, Yu Song, Chen Chen, Lina Zhao, Wanjie Ma, Shuqi Meng, Xiaoli Zhuang, Huayi Lin, Jing Liang, Yan Cui, Keliang Xie
Journal: International Immunopharmacology
Year: 2023
DOI: 10.1016/j.intimp.2022.109603
Study Type: Mouse
Outcome: Positive
Peer Reviewed: Yes
Country: China
Health Condition: Sepsis
Body System: Nervous System

TL;DR

Inhaling molecular hydrogen (H2) helps improve survival and brain function in mice with sepsis-related brain damage by reducing harmful protein changes and inflammation in the brain.

Key Finding

Mice with sepsis-induced cognitive dysfunction that received molecular hydrogen inhalation showed improved survival rates, better memory and learning ability, and reduced tau protein accumulation in the brain compared to untreated septic mice.

Summary

This study tested whether inhaling molecular hydrogen (H2) could help mice recover from cognitive problems caused by sepsis (a serious infection). Researchers found that mice treated with hydrogen gas showed improved memory and learning, survived longer, and had healthier brain cells in the hippocampus (the memory center of the brain). The protective effect appeared to work by reducing the buildup of a protein called tau, which damages brain cells during sepsis.

Practical Takeaway

While this mouse study suggests molecular hydrogen may protect the brain during severe infection, it is very early-stage research that has not been tested in humans. Anyone interested in hydrogen as a potential sepsis treatment should understand that animal studies often do not translate directly to human benefit, and clinical trials would be needed before any therapeutic claims could be made.

Abstract

Background: Sepsis-associated encephalopathy (SAE) is a cognitive dysfunction caused by sepsis. Hyperphosphorylated tau is considered to play a significant role in the progression of neurodegenerative disease and also contributes to cognitive dysfunction in septic mice. Molecular hydrogen (H2) plays an antioxidant and anti-inflammatory role, and plays a protective role in septic mice. This study explored the possible effects of H2 on cognition and tau phosphorylation in a mouse model of SAE. Methods: The model of sepsis was established in C57BL/6J male mice by cecal ligation and puncture surgery. Mice treated with 2 % H2 inhalation for 60 min at 1 h and 6 h after surgery, respectively. HY-15769, the inhibitor of Tau Tubulin Kinase 1 (TTBK1), was injected 1 h before the surgery. The 7-day survival rates of the mice were recorded. Cognitive behavior was tested with both novel object recognition and the Y-maze novelty arm recognition on day 7 after surgery. Hematoxylin-eosin staining was used to observe the histological damage in CA1 region of hippocampus. The expression of inflammatory factors in hippocampus was assessed by Elisa. Western blotting was adopted to determine the tau phosphorylation levels at AT8 epitopes (pSer202 and pThr205) and T22 epitopes (neurofibrillary tangle protein oligomer), and the GSK3β phosphorylation levels (Tyr216), as well as p-Ser422 and TTBK1 levels in the hippocampus. The number of dendritic spine and mushroom type of dendritic spines in the hippocampus were assessed by Golgi staining. Results: The survival rate, visual and spatial learning ability, and memory ability were improved in septic mice treated with H2. After H2 treatment, the density of dendritic spine, mushroom type of dendritic spine, and the number of normal hippocampal neurons were progressively elevated. H2 decreased the levels of phosphorylated tau protein, tau oligomer and TTBK1, as well as the phosphorylation of tau key kinase. Furthermore, the injection of HY-15769 (a TTBK1 inhibitor) protected SAE through the similar way. Conclusion: The protective effect of H2 on cognitive dysfunction induced by SAE may be achieved by inhibiting tau phosphorylation, which is perhaps related with the inhibition of TTBK1.