Hydrogen Water Protects Brain After Hemorrhagic Stroke in Animal Study
- Authors
- Zong Zhuang, Xue-Jun Sun, Xing Zhang, Huan-Dong Liu, Wan-Chun You, Chi-Yuan Ma, Lin Zhu, Meng-Liang Zhou, Ji-Xin Shi
- Journal
- Journal of Neuroscience Research
- Year
- 2013
- DOI
- 10.1002/jnr.23281
- Study Type
- Rabbit
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Subarachnoid Hemorrhage
- Body System
- Nervous System
TL;DR
Hydrogen treatment reduces brain damage and neuron death after a brain hemorrhage by activating a protective pathway in the brain.
Key Finding
Hydrogen-rich saline treatment reduced brain cell death and neuronal apoptosis (programmed cell death) in rabbits with simulated subarachnoid hemorrhage by activating a specific protective cellular pathway.
Summary
This study tested whether hydrogen-rich saline could protect rabbit brains from injury caused by simulated subarachnoid hemorrhage (bleeding in the space around the brain). Researchers found that hydrogen treatment reduced brain cell death by activating a protective pathway called NF-κB/Bcl-xL, which helps neurons survive.
Practical Takeaway
While this animal study suggests hydrogen may have neuroprotective properties in brain injury, it is a rabbit study only and does not directly demonstrate effects in humans. Much more research, including human clinical trials, would be needed before any therapeutic claims could be made for stroke or brain hemorrhage patients.
Abstract
Early brain injury (EBI), a significant contributor to poor outcome after subarachnoid hemorrhage (SAH), is intimately associated with neuronal apoptosis. Recently, the protective role of hydrogen (H2) in the brain has been widely studied, but the underlying mechanism remains elusive. Numerous studies have shown nuclear factor‐κB (NF‐κB) as a crucial survival pathway in neurons. Here we investigated the role of H2in EBI following SAH, focusing on the NF‐κB pathway. A double blood injection model was used to produce experimental SAH, and H2‐rich saline was injected intraperitoneally. NF‐κB activity within the occipital cortex was measured. Immunofluorescence was performed to demonstrate the activation of NF‐κB; Bcl‐xL and cleaved caspase‐3 were determined via Western blot. Gene expression of Bcl‐xL was detected by real‐time PCR, and TUNEL and Nissl staining were performed to illustrate brain injury in the occipital cortex. SAH induced a significant increase of cleaved caspase‐3. Correspondingly, TUNEL staining demonstrated obvious neuronal apoptosis following SAH. In contrast, H2treatment markedly increased NF‐κB activity and the expression of Bcl‐xL and decreased the level of cleaved caspase‐3. Additionally, H2treatment significantly reduced post‐SAH neuronal apoptosis. The current study shows that H2treatment alleviates EBI in the rabbits following SAH and that NF‐κB/Bcl‐xL pathway is involved in the protective role of H2. © 2013 Wiley Periodicals, Inc.