Hydrogen Gas Protects Brain After Stroke in Rats
- Authors
- Kai Zhuang, Yu-Chun Zuo, Prativa Sherchan, Ji-Kai Wang, Xiao-Xin Yan, Fei Liu
- Journal
- Frontiers in Neuroscience
- Year
- 2020
- DOI
- 10.3389/fnins.2019.01441
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Subarachnoid Hemorrhage
- Body System
- Nervous System
TL;DR
Inhaling hydrogen gas can reduce brain damage and improve recovery in rats after a type of stroke caused by bleeding in the brain.
Key Finding
Hydrogen inhalation at 3.3% concentration reduced brain damage, swelling, and blood clots while improving neurological recovery in rats with subarachnoid hemorrhage, apparently by reducing harmful free radicals and inflammatory responses.
Summary
Researchers tested whether inhaling hydrogen gas could protect the brain after a type of stroke called subarachnoid hemorrhage in rats. They found that hydrogen inhalation reduced brain swelling, blood clots in small vessels, and improved recovery by decreasing harmful molecules called free radicals and reducing inflammation in blood vessel cells.
Practical Takeaway
This rat study suggests hydrogen inhalation may have protective effects against brain injury from a specific type of stroke, but it is early-stage research in animals only. Human studies would be needed to determine if these benefits apply to people, and this should not be considered a treatment for stroke at this time.
Abstract
Background: Subarachnoid hemorrhage (SAH) is a devastating cerebrovascular disease with poor clinical outcome. Nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome serves a key role in inflammatory response, which may lead to endothelial cell injury and blood-brain barrier (BBB) disruption. Hydrogen (H2) is considered a neuroprotective antioxidant. This study was set out to explore whether hydrogen inhalation protects against SAH induced endothelial cell injury, BBB disruption, microthrombosis and vasospasm in rats. Methods: One hundred eighty-two male SD rats were used for the study. SAH was induced by endovascular perforation. H2 at a concentration of 3.3% was inhaled beginning at 0.5 h after SAH for duration of 30, 60 or 120 min, followed by single administration or once daily administration for 3 days. The temporal expression of NLRP3 and ASC in the brain was determined, with the effect of hydrogen inhalation evaluated. In addition, brain water content, oxidative stress markers, inflammasome, apoptotic markers, microthrombosis, and vasospasm were evaluated at 24 or 72 h after SAH. Results: The expression of NLRP3 and ASC were upregulated after SAH associated with elevated expression of MDA, 8-OHdG, 4-HNE, HO-1, TLR4/NF-κB, inflammatory and apoptotic makers. Hydrogen inhalation reduced the expression of these inflammatory and apoptotic makers in the vessels, brain edema, microthrombi formation, and vasospasm in rats with SAH relative to control. Hydrogen inhalation also improved short-term and long-term neurological recovery after SAH. Conclusion: Hydrogen inhalation can ameliorate oxidative stress related endothelial cells injury in the brain and improve neurobehavioral outcomes in rats following SAH. Mechanistically, the above beneficial effects might be related to, at least in part, the inhibition of activation of ROS/NLRP3 axis.