Hydrogen Therapy Protects Brain After Stroke-Like Brain Bleeding
- Authors
- Yuan Hong, AnWen Shao, Jianfeng Wang, Sheng Chen, HaiJian Wu, Devin W. McBride, Qun Wu, XueJun Sun, JianMin Zhang
- Journal
- PLoS One
- Year
- 2014
- DOI
- 10.1371/journal.pone.0096212
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Subarachnoid Hemorrhage
- Body System
- Nervous System
TL;DR
Hydrogen-rich saline can reduce brain cell death and improve brain function after a type of stroke known as subarachnoid hemorrhage, possibly by activating a protective signaling pathway in the brain.
Key Finding
Hydrogen-rich saline significantly reduced brain cell death and improved neurological function in rats with subarachnoid hemorrhage by activating a protective cellular pathway called Akt/GSK3β.
Summary
Researchers tested whether hydrogen-rich saline could protect rat brains from damage after a type of stroke called subarachnoid hemorrhage. They found that hydrogen-rich saline reduced brain cell death and improved neurological function in treated rats compared to untreated ones, and identified a specific cellular pathway (Akt/GSK3β) that appears to be responsible for this protective effect.
Practical Takeaway
This rat study provides early evidence that hydrogen may protect brain cells from damage in certain types of stroke, but it is not yet known whether these results apply to humans. Much more research, including human clinical trials, would be needed before hydrogen-rich saline could be considered a treatment for stroke.
Abstract
Backgrounds: Early brain injury (EBI) plays a key role in the pathogenesis of subarachnoid hemorrhage (SAH). Neuronal apoptosis is involved in the pathological process of EBI. Hydrogen can inhibit neuronal apoptosis and attenuate EBI following SAH. However, the molecular mechanism underlying hydrogen-mediated anti-apoptotic effects in SAH has not been elucidated. In the present study, we aimed to evaluate whether hydrogen alleviates EBI after SAH, specifically neuronal apoptosis, partially via the Akt/GSK3β signaling pathway. Methods: Sprague-Dawley rats (n = 85) were randomly divided into the following groups: sham group (n = 17), SAH group (n = 17), SAH + saline group (n = 17), SAH + hydrogen-rich saline (HS) group (n = 17) and SAH + HS + Ly294002 (n = 17) group. HS or an equal volume of physiological saline was administered immediately after surgery and repeated 8 hours later. The PI3K inhibitor, Ly294002, was applied to manipulate the proposed pathway. Neurological score and SAH grade were assessed at 24 hours after SAH. Western blot was used for the quantification of Akt, pAkt, GSK3β, pGSK3β, Bcl-2, Bax and cleaved caspase-3 proteins. Neuronal apoptosis was identified by double staining of terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining and NeuN, and quantified by apoptosis index. Immunohistochemistry and immunofluorescent double-labeling staining was performed to clarify the relationships between neuronal apoptosis and pAkt or pGSK3β. Results: HS significantly reduced neuronal apoptosis and improved neurological function at 24 hours after SAH. The levels of pAkt and pGSK3β, mainly expressed in neurons, were markedly up-regulated. Additionally, Bcl-2 was significantly increased while Bax and cleaved caspase-3 was decreased by HS treatment. Double staining of pAkt and TUNEL showed few colocalization of pAkt-positive cells and TUNEL-positive cells. The inhibitor of PI3K, Ly294002, suppressed the beneficial effects of HS. Conclusions: HS could attenuate neuronal apoptosis in EBI and improve the neurofunctional outcome after SAH, partially via the Akt/GSK3β pathway.