New Hydrogen Treatment Protects Brain After Stroke in Animal Study
- Authors
- Weijian Fan, Qingqing Guan, Zhiheng Xu, Lanmei Lin, Juan Du, Bo Yu, Wenjiang Ding, Haiyan Yang, Jia Pei, Jinyun Tan
- Journal
- Advanced Healthcare Materials
- Year
- 2025
- DOI
- 10.1002/adhm.202502482
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Cerebral Ischemia/Reperfusion Injury
- Body System
- Nervous System
TL;DR
Magnesium hydride microparticles delivered hydrogen to the brain, reducing oxidative stress and protecting neurons by improving mitochondrial function after ischemia-reperfusion injury.
Key Finding
Magnesium hydride microparticles successfully delivered sustained, high-dose hydrogen to the brain and reduced reactive oxygen species while protecting brain cells from ferroptosis and restoring mitochondrial function in a rabbit model of cerebral ischemia/reperfusion injury.
Summary
This study tested a new way to deliver hydrogen gas to the brain using magnesium hydride microparticles (tiny particles that slowly release hydrogen) in rabbits with a type of brain injury caused by temporarily blocking blood flow to the brain. The researchers found that this hydrogen delivery method reduced harmful molecules called reactive oxygen species, protected brain cells from a type of damage called ferroptosis, and restored normal function to mitochondria (the energy-producing parts of cells).
Practical Takeaway
This is early-stage research in animals only, not humans. While the results suggest that sustained hydrogen delivery to the brain may have neuroprotective effects in stroke-like injuries, much more research—including human trials—would be needed before this approach could be considered for treating stroke or brain injury in people. The delivery method itself is novel and addresses previous challenges in getting hydrogen across the blood-brain barrier, but safety and effectiveness in humans remain unknown.
Abstract
Mitochondrial dysfunction and reactive oxygen species (ROS) overexpression are crucial factors inducing neuronal ferroptosis in cerebral ischemia/reperfusion injury (CIRI). Some therapeutics like RNAs and anti-oxidation drugs have been developed to regulate the functions of mitochondria, but are hardly delivered into brain effectively due to the blood-brain barrier (BBB). H2 has recently been verified able to overcome the BBB efficiently and has a unique wide-spectrum anti-oxidation/anti-inflammation effect, but sustainable, high-amount, and safe delivery of H2 into brain is still challenging currently. Herein, we develop an innovative H2 administration method of intraperitoneal injection of magnesium hydride microparticles (MgH2) with a high payload of hydrogen and a sustained hydrolytic H2 production behavior, achieving persistent and high-dose supply of H2 into the blood system as well as in the brain. In addition, we establish a novel CIRI rabbit model induced by transcarotid artery revascularization (TCAR), which leads to oxidative stress and subsequent ferroptosis in the brain's hippocampus. In this CIRI model, MgH2 treatment eliminates intracellular ROS, inhibits neuronal ferroptosis, and recovers mitochondrial dysfunction by stabilizing mitochondrial membrane potential, regulating mitobiogenesis, promoting neuronal energy metabolism, and activating the anti-oxidative pathway. All these findings demonstrate that MgH2 treatment provides a potential strategy for CIRI.