Hydrogen Gas Helps Brain Recovery After Head Injury in Rats
- Authors
- Lu Wang, Chongfa Zhao, Shuang Wu, Guanghui Xiao, Xin Zhuge, Ping Lei, Ke-Liang Xie
- Journal
- Shock
- Year
- 2018
- DOI
- 10.1097/SHK.0000000000001018
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Traumatic Brain Injury
- Body System
- Nervous System
TL;DR
Hydrogen gas treatment helps improve brain function after a traumatic brain injury by boosting levels of a beneficial molecule called miR-21.
Key Finding
Hydrogen gas treatment improved neurological outcomes after traumatic brain injury in rats by increasing microRNA-21 expression, which reduced brain swelling, decreased lesion size, and enhanced the brain's natural antioxidant defenses.
Summary
This rat study tested whether hydrogen gas could help recovery from traumatic brain injury (TBI) by increasing a molecule called microRNA-21 (miR-21). Rats with brain injuries were exposed to hydrogen gas, and researchers found that hydrogen increased miR-21 levels in the brain and improved neurological function, reduced brain swelling, and decreased brain damage. When researchers blocked miR-21, hydrogen's protective effects disappeared, suggesting that miR-21 is essential for hydrogen's benefits.
Practical Takeaway
This is an early-stage animal study showing a potential mechanism by which hydrogen gas might help brain injury recovery. However, it was conducted only in rats, and the results do not yet indicate whether hydrogen would be effective or safe in humans with brain injuries. Much more research, including human clinical trials, would be needed before any therapeutic recommendations could be made.
Abstract
Hydrogen gas (H2) exerts a beneficial effect against traumatic brain injury (TBI). microRNA-21 (miR-21) is one of the most highly expressed members of small non-coding microRNA family in mammalian cells. miR-21 can improve the neurological outcome after TBI. In the present study, we investigated whether H2 treatment could improve the neurological outcome after TBI via increasing miR-21 expression. TBI was induced by controlled cortical impact in rats. H2 treatment was given by exposure to 2% H2 from 30 min to 5 h after TBI operation. Here, we found that H2 treatment significantly increased the expression of miR-21 in brain from 6 h to 3 d after TBI. The level of miR-21 expression in brain was significantly decreased after intracerebroventricular infusion of miR-21 antagomir in TBI-challenged rats with or without H2 treatment. Moreover, we found that H2 treatment conferred a better neurological outcome after TBI by improving neurological dysfunction, alleviating brain edema as well as decreasing lesion volume and blood-brain barrier permeability, which were significantly prevented by miR-21 antagomir. Furthermore, intracerebroventricular infusion of miR-21 agomir increased the level of miR-21 expression and decreased the lesion volume after TBI. In addition, H2 treatment decreased the levels of oxidative products (malondialdehyde and 8-iso-prostaglandin F2α) and increased the activities of endogenous antioxidant enzymes (superoxide dismutase and catalase) in brain after TBI, which were prevented by miR-21 antagomir. Taken together, these data indicate that H2 treatment improves the neurological outcome after TBI via increasing miR-21 expression.