Hydrogen Gas Protects Brain After Stroke by Blocking Harmful Immune Cells
- Authors
- Anatol Manaenko, Tim Lekic, Qingyi Ma, John H. Zhang, Jiping Tang
- Journal
- Critical Care Medicine
- Year
- 2013
- DOI
- 10.1097/CCM.0b013e31827711c9
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- United States
- Health Condition
- Intracerebral Hemorrhage
- Body System
- Nervous System
TL;DR
Breathing in hydrogen gas can protect the brain and improve recovery after a stroke by preventing immune cells called mast cells from causing further damage.
Key Finding
Hydrogen inhalation reduced mast cell activation and prevented blood-brain barrier breakdown in mice with intracerebral hemorrhage, leading to less brain swelling and better neurological outcomes.
Summary
Researchers gave mice with brain bleeding hydrogen gas to breathe and studied how it affected brain injury. They found that hydrogen reduced activation of mast cells (immune cells in the brain), which helped protect the blood-brain barrier (the membrane that controls what enters the brain), reduced brain swelling, and improved neurological function in the mice.
Practical Takeaway
This is an early-stage animal study showing hydrogen may help protect the brain after bleeding by reducing immune cell activation. However, these results are from mice only and have not been tested in humans, so it is too soon to draw conclusions about hydrogen's usefulness for stroke patients.
Abstract
Objective: Hydrogen inhalation was neuroprotective in several brain injury models. Its mechanisms are believed to be related to antioxidative stress. We investigated the potential neurovascular protective effect of hydrogen inhalation especially effect on mast cell activation in a mouse model of intracerebral hemorrhage. Design: Controlled in vivo laboratory study. Setting: Animal research laboratory. Subjects: One hundred seventy-one 8-week-old male CD-1 mice were used. Interventions: Collagenase-induced intracerebral hemorrhage model in 8-week-old male CD-1 mice was used. Hydrogen was administrated via spontaneous inhalation. The blood-brain barrier permeability and neurologic deficits were investigated at 24 and 72 hours after intracerebral hemorrhage. Mast cell activation was evaluated by Western blot and immuno-staining. The effects of hydrogen inhalation on mast cell activation were confirmed in an autologous blood injection model intracerebral hemorrhage. Measurement and main results: At 24 and 72 hours post intracerebral hemorrhage, animals showed blood-brain barrier disruption, brain edema, and neurologic deficits, accompanied with phosphorylation of Lyn kinase and release of tryptase, indicating mast cell activation. Hydrogen treatment diminished phosphorylation of Lyn kinase and release of tryptase, decreased accumulation and degranulation of mast cells, attenuated blood-brain barrier disruption, and improved neurobehavioral function. Conclusion: Activation of mast cells following intracerebral hemorrhage contributed to increase of blood-brain barrier permeability and brain edema. Hydrogen inhalation preserved blood-brain barrier disruption by prevention of mast cell activation after intracerebral hemorrhage.