Hydrogen Gas Protects Brain After Stroke in Rats
- Authors
- Chuan-Suo Zhang, Qian Han, Zhao-Wei Song, Hong-Yan Jia, Tian-Peng Shao, Yan-Peng Chen
- Journal
- Experimental and Therapeutic Medicine
- Year
- 2021
- DOI
- 10.3892/etm.2021.10268
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Subarachnoid Hemorrhage
- Body System
- Nervous System
TL;DR
Breathing hydrogen gas after a brain hemorrhage may protect brain cells by reducing inflammation and cell death through a specific cell signaling pathway.
Key Finding
Hydrogen gas inhalation for 2 hours after induced subarachnoid hemorrhage in rats reduced brain swelling, improved neurological function, and decreased neuronal cell death by activating protective cellular pathways and reducing oxidative stress.
Summary
This rat study tested whether breathing hydrogen gas after a type of stroke caused by a ruptured blood vessel in the brain could reduce brain damage. Researchers found that rats treated with hydrogen gas for 2 hours after the stroke had less brain swelling, better neurological function, and reduced cell death compared to untreated rats. The protective effect appeared to work through specific cellular pathways (mitoKATP/ERK1/2/p38 MAPK) that control inflammation and oxidative stress (harmful chemical reactions in cells).
Practical Takeaway
While this rat study suggests hydrogen gas may have neuroprotective effects after certain types of stroke, it is a preliminary animal study that does not directly translate to human treatment. Much more research, including human clinical trials, would be needed before hydrogen gas could be considered a viable therapy for stroke patients. The findings may warrant further investigation but should not be interpreted as evidence of benefit in humans.
Abstract
Neuronal pyroptosis serves an important role in the progress of neurologic dysfunction following subarachnoid hemorrhage (SAH), which is predominantly caused by a ruptured aneurysm. Hydrogen gas has been previously reported to be an effective anti-inflammatory agent against ischemia-associated diseases by regulating mitochondrial function. The objective of the present study was to investigate the potential neuroprotective effects of hydrogen gas post-conditioning against neuronal pyroptosis after SAH, with specific focus on the mitochondrial ATP-sensitive K+ (mitoKATP) channels. Following SAH induction by endovascular perforation, rats were treated with inhalation of 2.9% hydrogen gas for 2 h post-perforation. Neurologic deficits, brain water content, reactive oxygen species (ROS) levels, neuronal pyroptosis, phosphorylation of ERK1/2, p38 MAPK and pyroptosis-associated proteins IL-1β and IL-18 were evaluated 24 h after perforation by a modified Garcia method, ratio of wet/dry weight, 2',7'-dichlorofluorescin diacetate, immunofluorescence and western blot assays, respectively. An inhibitor of the mitoKATP channel, 5-hydroxydecanoate sodium (5-HD), was used to assess the potential role of the mitoKATP-ERK1/2-p38 MAPK signal pathway. Hydrogen gas post-conditioning significantly alleviated brain edema and improved neurologic function, reduced ROS production and neuronal pyroptosis, suppressed the expression of IL-1β and IL-18 whilst upregulating ERK1/2 phosphorylation, but downregulated p38 MAPK activation 24 h post-SAH. These aforementioned effects neuroprotective were partially reversed by 5-HD treatment. Therefore, these observations suggest that post-conditioning with hydrogen gas ameliorated SAH-induced neuronal pyroptosis at least in part through the mitoKATP/ERK1/2/p38 MAPK signaling pathway.