Hydrogen Therapy Protects Brain and Memory After Severe Seizures
- Authors
- Ruihua Jia, Ning Jia, Fang Yang, Zihe Liu, Rui Li, Yongli Jiang, Jingjing Zhao, Lu Wang, Shuo Zhang, Zhengping Zhang, Haifeng Zhang, Shengxi Wu, Fang Gao, Wen Jiang
- Journal
- Cellular and Molecular Neurobiology
- Year
- 2019
- DOI
- 10.1007/s10571-019-00685-5
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Status Epilepticus
- Body System
- Nervous System
TL;DR
Hydrogen treatment helps protect brain cells and improve learning and memory in rats that have experienced prolonged seizures.
Key Finding
Hydrogen treatment improved memory and learning deficits in rats with status epilepticus by reducing neuronal death through multiple protective mechanisms.
Summary
This study tested whether hydrogen gas could protect the brain in rats with status epilepticus (prolonged, uncontrolled seizures). Researchers found that hydrogen treatment improved memory and learning in affected rats and reduced the death of brain cells by blocking two cell-death pathways (necroptosis and apoptosis). Hydrogen also reduced inflammation from immune cells in the brain.
Practical Takeaway
This early-stage animal study suggests hydrogen may have neuroprotective effects against seizure-related brain damage, but it is far too preliminary to inform human treatment decisions. The research was conducted only in rats, and no human trials have been conducted. Much more research, including human studies, would be needed before hydrogen could be considered a clinical treatment for seizure-related cognitive problems.
Abstract
Status epilepticus without prompt seizure control always leads to neuronal death and long-term cognitive deficits, but effective intervention is still absent. Here, we found that hydrogen could alleviate the hippocampus-dependent spatial learning and memory deficit in lithium–pilocarpine model of status epilepticus in rats, as evidenced by the results in Morris water maze test. Hydrogen treatment downregulated the expression of necroptosis-related proteins, such as MLKL, phosphorylated-MLKL, and RIPK3 in hippocampus, and further protected neurons and astrocytes from necroptosis which was here first verified to occur in status epilepticus. Hydrogen also protected cells from apoptosis, which was indicated by the decreased cleaved-Caspase 3 expression. Meanwhile, Iba1⁺ microglial activation by status epilepticus was reduced by hydrogen treatment. These findings confirm the utility of hydrogen treatment in averting cell death including necroptosis and alleviating cognitive deficits caused by status epilepticus. Therefore, hydrogen may provide a potential and powerful clinical treatment for status epilepticus-related cognitive deficits.