Hydrogen Gas Protects Brain Function After Sepsis in Mice
- Authors
- Yi Jiang, Kai Zhang, Yang Yu, Yaoqi Wang, Naqi Lian, Keliang Xie, Yong-Hao Yu
- Journal
- Experimental Brain Research
- Year
- 2020
- DOI
- 10.1007/s00221-020-05950-4
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Sepsis
- Body System
- Nervous System
TL;DR
Inhaling hydrogen gas can help reduce brain damage and improve brain function in mice with sepsis-related brain injuries.
Key Finding
In mice with sepsis-induced brain injury, inhaling 2% hydrogen gas improved survival rates, reduced cognitive impairment, and decreased brain damage markers compared to untreated septic mice.
Summary
This study tested whether inhaling hydrogen gas could protect the brains of mice with sepsis (a severe infection). Researchers gave mice either a placebo or 2% hydrogen gas to breathe after inducing sepsis, then measured survival rates, memory and learning ability, and markers of brain damage. Mice that received hydrogen gas had better survival rates, performed better on memory tests, showed less brain tissue damage, and had lower levels of inflammatory chemicals in their brains compared to mice that didn't receive hydrogen.
Practical Takeaway
While this mouse study suggests hydrogen gas may help protect the brain during severe infection, it is important to note this was conducted only in animals and has not been tested in humans. Much more research, including human clinical trials, would be needed before hydrogen therapy could be considered a treatment for sepsis-related brain injury in people.
Abstract
Sepsis-related encephalopathy (SAE), which causes a series of brain injuries and long-term, potentially irreversible cognitive dysfunction, is closely associated with increased morbidity and mortality. Hydrogen (H2) is a new type of medical gas molecule that has been widely used in the treatment of various diseases in recent years. The aim of the present study was to explore the protective effects of H2 inhalation on brain injury and long-term cognitive impairment in an improved chronic septic mouse model. Male C57BL/6J mice were randomized into four groups: Control, Control + H2, SAE and SAE + H2. The SAE and Control models were established by intraperitoneal injection of human stool suspension or saline in mice. H2 (2%) was inhaled for 60 min at 1 h and 6 h after SAE or Control treatment. The survival rates were recorded for 14 days (days 1-14) and the Morris Water Maze was performed for 7 days (days 8-14). To assess the severity of the brain injury, hematoxylin and eosin staining, Nissl staining, Evans blue (EB) extravasation and the wet/dry weight ratio of brain tissue were detected 24 h after SAE or Control treatment. In addition, inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin 6 (IL-6), high-mobility group box 1 (HMGB1), as well as the protein levels of nuclear factor-erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), zonula occludens-1 (ZO-1) and Occludin, were measured 6, 12 and 24 h after SAE or Control treatment. The results showed that H2 treatment increased survival rates, mitigated cognitive impairment, reduced hippocampal histological damage, decreased EB and water content, and decreased the levels of TNF-α, IL-6, HMGB1, Nrf2, HO-1, ZO-1 and Occludin, as compared with the SAE group. These data revealed that 2% H2 could suppress brain damage and improve cognitive function in septic mice by inhibiting oxidative stress, inflammatory response and the sepsis-induced blood-brain barrier (BBB) disruption.