Hydrogen Gas Reduces Brain Bleeding in Stroke Rats with High Blood Sugar
- Authors
- C.H. Chen, A. Manaenko, Y. Zhan, W.W. Liu, R.P. Ostrowki, J. Tang, J.H. Zhang
- Journal
- Neuroscience
- Year
- 2011
- DOI
- 10.1016/j.neuroscience.2010.04.043
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- United States
- Health Condition
- Ischemic Stroke
- Body System
- Neurological
TL;DR
Breathing in hydrogen gas reduced brain damage and improved recovery in rats that had a type of stroke caused by a blocked artery.
Key Finding
Hydrogen gas inhalation reduced brain damage and bleeding in rats with stroke and high blood sugar, while also improving neurological function.
Summary
Researchers tested whether hydrogen gas could help protect rat brains from damage after a stroke, especially when blood sugar levels were high. Rats that received hydrogen gas through inhalation after a stroke showed smaller areas of brain damage, less bleeding in the brain, and better neurological function compared to rats that didn't receive hydrogen. The hydrogen appeared to work by reducing harmful molecules called oxidative stress markers and lowering blood glucose levels.
Practical Takeaway
This rat study suggests hydrogen gas may help protect the brain during stroke, particularly in people with high blood sugar. However, this is early-stage animal research, and it's unclear whether these results would apply to humans or what the optimal dose and timing would be. Much more research, including human trials, would be needed before hydrogen could be considered a stroke treatment.
Abstract
Hyperglycemia is one of the major factors for hemorrhagic transformation after ischemic stroke. In this study, we tested the effect of hydrogen gas on hemorrhagic transformation in a rat focal cerebral ischemia model. Sprague-Dawley rats (n=72) were divided into the following groups: sham; sham treated with hydrogen gas (H(2)); Middle Cerebral Artery Occlusion (MCAO); and MCAO treated with H(2) (MCAO+H(2)). All rats received an injection of 50% dextrose (6 ml/kg i.p.) and underwent MCAO 15 min later. Following a 90 min ischemic period, hydrogen was inhaled for 2 h during reperfusion. We measured the level of blood glucose at 0 h, 0.5 h, 4 h, and 6 h after dextrose injection. Infarct and hemorrhagic volumes, neurologic score, oxidative stress (evaluated by measuring the level of 8 Hydroxyguanosine (8OHG), 4-Hydroxy-2-Nonenal (HNE) and nitrotyrosine), and matrix metalloproteinase (MMP)-2/MMP-9 activity were measured at 24 h after ischemia. We found that hydrogen inhalation for 2 h reduced infarct and hemorrhagic volumes and improved neurological functions. This effect of hydrogen was accompanied by a reduction of the expression of 8OHG, HNE, and nitrotyrosine and the activity of MMP-9. Furthermore, a reduction of the blood glucose level from 500+/-32.51 to 366+/-68.22 mg/dl at 4 h after dextrose injection was observed in hydrogen treated animals. However, the treatment had no significant effect on the expression of ZO-1, occludin, collagen IV or aquaporin4 (AQP4). In conclusion, hydrogen gas reduced brain infarction, hemorrhagic transformation, and improved neurological function in rats. The potential mechanisms of decreased oxidative stress and glucose levels after hydrogen treatment warrant further investigation.