Hydrogen Water Protects Brain Function in Young Rats with Sepsis
- Authors
- John Sieh Dumbuya, Siqi Li, Lili Liang, Yanchen Chen, Jiang Du, Qiyi Zeng
- Journal
- Journal of Translational Medicine
- Year
- 2022
- DOI
- 10.1186/s12967-022-03746-4
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Sepsis-Associated Encephalopathy
- Body System
- Nervous System
TL;DR
A study found that injecting a solution containing hydrogen gas can reduce brain inflammation, protect nerve cells, and improve survival in young rats with a brain condition caused by severe infection.
Key Finding
In young rats with sepsis-associated encephalopathy, hydrogen-rich saline treatment reduced brain inflammation, decreased cell death, and restored mitochondrial function compared to untreated animals.
Summary
This study tested whether hydrogen-rich saline (a salt water solution containing molecular hydrogen) could protect the brains of young rats with sepsis-associated encephalopathy—a serious brain condition that develops during severe infection. Researchers gave rats an infection-triggering substance, then treated some with hydrogen-rich saline. The treated rats showed less brain cell damage, reduced inflammation, fewer dying brain cells, and better functioning of mitochondria (the energy-producing parts of cells) compared to untreated rats.
Practical Takeaway
This is early-stage animal research only—it has not been tested in humans. The findings suggest hydrogen-rich saline may have protective effects on the brain during severe infection, but much more research, including human trials, would be needed before any therapeutic use could be considered. The study's relevance to healthy people or those using hydrogen water is unclear.
Abstract
Background: Sepsis-associated encephalopathy (SAE) is one of the most common types of sepsis-related organ dysfunction without overt central nervous system (CNS) infection. It is associated with higher mortality, low quality of life, and long-term neurological sequelae in suspected patients. At present there is no specific treatment for SAE rather than supportive therapy and judicious use of antibiotics, which are sometimes associated with adverse effects. Molecular hydrogen (H2) has been reported to play crucial role in regulating inflammatory responses, neuronal injury, apoptosis and mitochondrial dysfunction in adult models of SAE. Here we report the protective effect of hydrogen-rich saline in juvenile SAE rat model and its possible underling mechanism(s). Materials and methods: Rats were challenged with lipopolysaccharide (LPS) at a dose of 8 mg/kg injected intraperitoneally to induce sepsis and hydrogen-rich saline (HRS) administered 1 h following LPS induction at a dose of 5 ml/kg. Rats were divided into: sham, sham + HRS, LPS and LPS + HRS. At 48 h, rats were sacrificed and Nissl staining for neuronal injury, TUNEL assay for apoptotic cells detection, immunohistochemistry, and ELISA protocol for inflammatory cytokines determination, mitochondrial dysfunction parameters, electron microscopy and western blot analysis were studied to examine the effect of HRS in LPS-induced septic rats. Results: Rats treated with HRS improved neuronal injury, improvement in rats' survival rate. ELISA analysis showed decreased TNF-α and IL-1β and increased IL-10 expression levels in the HRS-treated group. Apoptotic cells were decreased after HRS administration in septic rats. The numbers of GFAP and IBA-1positive cells were attenuated in the HRS-treated group when compared to the LPS group. Subsequently, GFAP and IBA-1 immunoreactivity were decreased after HRS treatment. Mitochondrial membrane potential detected by JC-1 dye and ATP content were decreased in septic rats, which were improved after HRS treatment, while release of ROS was increased in the LPS group reverted by HRS treatment, ameliorating mitochondrial dysfunction. Further analysis by transmission electron microscopy showed decreased number of mitochondria and synapses, and disrupted mitochondrial membrane ultrastructure in the LPS group, while HRS administration increased mitochondria and synapses number. Conclusion: These data demonstrated that HRS can improve survival rate, attenuate neuroinflammation, astrocyte and microglial activation, neuronal injury and mitochondrial dysfunction in juvenile SAE rat model, making it a potential therapeutic candidate in treating paediatric SAE. Keywords: Apoptosis; Astrocyte; Microglia; Mitochondrial dysfunction; Neuroinflammation; Neuronal injury; Paediatrics; Sepsis-associated encephalopathy.