Hydrogen Gas Protects Brain from Sepsis-Related Damage
- Authors
- Hongguang Chen, Beibei Dong, Yuan Shi, Yonghao Yu, Ke-Liang Xie
- Journal
- Neuroscience
- Year
- 2021
- DOI
- 10.1016/j.neuroscience.2021.05.003
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Sepsis-Associated Encephalopathy
- Body System
- Nervous System
TL;DR
Hydrogen gas (H2) helps protect the brain from inflammation and damage during sepsis by activating a protective pathway known as Nrf2.
Key Finding
Hydrogen gas reduced brain inflammation and protected nerve cells from damage in sepsis-associated encephalopathy by activating the Nrf2 signaling pathway, but these protective effects disappeared in mice genetically lacking the Nrf2 pathway.
Summary
This study investigated how hydrogen gas might protect the brain during sepsis (a severe infection that affects the whole body), specifically looking at a condition called sepsis-associated encephalopathy where the brain becomes inflamed and damaged. Researchers used mouse models and laboratory-grown brain cells to test whether hydrogen could reduce brain inflammation and nerve cell damage. They found that hydrogen appeared to work by activating a protective pathway called Nrf2, which reduced harmful inflammation and prevented brain cells from dying.
Practical Takeaway
While this early laboratory research suggests hydrogen may have neuroprotective effects in sepsis-related brain injury, these findings are from animal models and cell cultures only—not human studies. The specific condition studied (sepsis-associated encephalopathy) is a severe medical emergency requiring hospital care, so these results cannot be applied to general wellness use of hydrogen water. More research, including human trials, would be needed before any clinical recommendations could be made.
Abstract
Objective: Sepsis-associated encephalopathy (SAE) is characterized by diffuse cerebral and central nervous system (CNS) dysfunction. Microglia play a vital role in protecting the brain from neuronal damage, which is closely related to inflammatory responses. The Nrf2 signaling pathway has an impact on microglial and neuronal injury. Here, we mainly explored the molecular mechanism by which H2 regulates neuroinflammation in SAE and the role of Nrf2 in this process. Methods: An in vivo model of SAE was generated by cecal ligation and puncture (CLP). Primary microglia and neurons were cultured to establish an in vitro model. Microglia, neurons and brain tissue were obtained to detect Nrf2 expression, inflammation, cell injury, apoptosis, and microglial polarization. Escape latency, the number of platform crossings and the time spent in the target quadrant were measured to assess cognitive function. Results: H2 attenuated microglial polarization from the M1 to the M2 phenotype, cytokine release and TLR/NF-κb activation and protected neurons from LPS-activated microglia-induced injury via the Nrf2 pathway. SAE activated Nrf2 expression, and H2 further improved Nrf2 expression in SAE mice. H2 alleviated microglial polarization from the M1 to the M2 phenotype and cytokine release in the cerebral cortex and improved neuronal injury or cognitive dysfunction in SAE mice and wild-type mice but not in Nrf2-/- mice. Conclusion: H2 exerts antineuroinflammatory effects associated with TLR4/NF-κB signaling activation and neuroprotective effects by inhibiting the excessive release of proinflammatory cytokines, neuronal loss and apoptosis in vitro and in vivo through the Nrf2 pathway.