Can hydrogen gas help with lung damage after brain injury?

Yes, this rat study found that inhaling hydrogen gas significantly reduced lung damage after traumatic brain injury. The hydrogen prevented harmful cell death and reduced inflammation in the lungs.

How does hydrogen gas protect the lungs after brain injury?

Hydrogen gas works by blocking two types of harmful cell death called pyroptosis and apoptosis. It also reduces inflammatory proteins that damage lung tissue after brain trauma.

What concentration of hydrogen gas was used in this study?

Researchers used a mixture of 42% hydrogen gas, 21% oxygen, and balanced nitrogen. Rats breathed this mixture for one hour per day after their brain injuries.

Is hydrogen gas therapy safe for brain injury patients?

This study suggests hydrogen inhalation is safe and beneficial, but it was only tested in rats. Human clinical trials would be needed to confirm safety and effectiveness in brain injury patients.

Could hydrogen therapy be used in hospital intensive care units?

The researchers believe hydrogen inhalation could be easily integrated into ICU care for brain injury patients. It's non-invasive and could help prevent serious lung complications.

Hydrogen Gas Helps Lung Damage After Brain Injury in Rats

Authors: Ting-Ting Li, Tian Sun, Yue-Zhen Wang, Qiang Wan, Wen-Zhi Li, Wan-Chao Yang
Journal: European Journal of Pharmacology
Year: 2021
DOI: 10.1016/j.ejphar.2021.174664
Study Type: Rat
Outcome: Positive
Peer Reviewed: Yes
Country: China
Health Condition: Traumatic Brain Injury
Body System: Nervous System

TL;DR

Inhaling hydrogen gas can help rats recover from lung damage caused by traumatic brain injury by reducing inflammation and cell death.

Key Finding

Rats that inhaled 42% hydrogen gas daily showed significantly improved lung function and reduced markers of cell death and inflammation compared to injured rats that did not receive hydrogen treatment.

Summary

This study tested whether breathing hydrogen gas could help rats recover from lung injury caused by traumatic brain injury. Researchers gave some injured rats hydrogen gas to breathe for 1 hour daily and compared them to injured rats that didn't receive hydrogen. The hydrogen-treated rats showed better lung function, less fluid buildup in their lungs, and lower levels of proteins and chemicals associated with cell damage and inflammation.

Practical Takeaway

While this rat study suggests hydrogen gas may help reduce lung injury after brain trauma by decreasing inflammation and cell death, it is early-stage animal research only. Human studies would be needed to determine if these results apply to people, and this should not be considered a proven treatment for traumatic brain injury or lung injury at this time.

Abstract

Background: Traumatic brain injury (TBI)-induced acute lung injury (ALI) is a critical condition, and inflammation and apoptosis play essential roles. Molecular hydrogen (H2) exerts anti-inflammatory and anti-apoptotic effects. Our previous work has shown that 42% H2 can improve TBI. In the current study, we tested the hypothesis that inhalation of hydrogen (42% H2, 21% O2, balanced nitrogen) for 1 h per day can improve TBI-induced ALI. Methods: Sprague-Dawley male rats were randomly divided into 3 groups. Except for the sham group (group S), rats were subjected to a fluid percussion injury (FPI) and the H2 treatment group were given inhaled hydrogen for 1 h per day. We evaluated the lung function, pyroptosis and apoptosis at 24 h, 48 h and 72 h. Results: Compared with group S, the rats in the TBI group (group T) showed obvious pulmonary edema after a TBI. Inhalation of high-concentration hydrogen significantly improved the rats. During this process, rats had some tendency to heal on their own, and H2 also accelerated the self-healing process. Lung injury scores, oxygenation index and pulmonary edema were consistent. Compared with group S, the pyroptosis-related proteins Caspase-1, apoptosis-associated speck-like protein containing CARD (ASC) and Gasdermin-D (GSDM-D) in the lung tissues of the rats in group T were significantly increased after a TBI. In the H2 treatment group (group H), these proteins were significantly decreased. The levels of IL-1β and IL-18 were significantly increased after TBI while in group H were significantly decreased. At the same time, cleaved caspase-3 and BCL-2/Bax were also changed after H2 treatment. These demonstrates the powerful ameliorating effect of H2 on pyroptosis, apoptosis and systemic inflammation. However, rats also had tendency to heal on their own, and H2 also accelerated the self-healing process at the same time. Conclusions: H2 improves TBI-ALI, and the mechanism may be due to the decrease of both pyroptosis and apoptosis and the alleviation of inflammation. These findings provide a reference and evidence for the use of H2 in TBI-ALI patients in the intensive care unit (ICU).