Hydrogen Gas Reduces Brain Damage After Stroke in Mice
- Authors
- Qi-Yong Mei, Qin Hu, Jun-Long Huang, Wen-Wu Liu, Anatol Manaenko, Xue-Jun Sun
- Journal
- Medical Gas Research
- Year
- 2019
- DOI
- 10.4103/2045-9912.266987
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Ischemic Stroke
- Body System
- Nervous System
TL;DR
Breathing in high concentrations of hydrogen gas can reduce brain damage and improve recovery after a stroke by calming down immune cells in the brain.
Key Finding
High-concentration hydrogen gas inhalation reduced brain injury and neurological dysfunction after stroke in mice by suppressing inflammatory activation of immune cells in the brain.
Summary
Researchers studied whether breathing high-concentration hydrogen gas could protect the brain after a stroke in mice. They induced a stroke by blocking blood flow to part of the brain, then gave some mice hydrogen gas to breathe while others received a control gas. The hydrogen-treated mice had less brain damage, better neurological function, and showed changes in brain immune cells (microglia) that reduced inflammation.
Practical Takeaway
This mouse study suggests hydrogen gas may protect the brain after stroke by reducing inflammation, but this is early-stage research in animals only. Much more work—including human studies—would be needed before any conclusions about hydrogen's effects in stroke patients could be drawn.
Abstract
Microglia participate in bi-directional control of brain repair after stroke. Previous studies have demonstrated that hydrogen protects brain after ischemia/reperfusion (I/R) by inhibiting inflammation, but the specific mechanism of anti-inflammatory effect of hydrogen is poorly understood. The goal of our study is to investigate whether inhalation of high concentration hydrogen (HCH) is able to attenuate I/R-induced microglia activation. Eighty C57B/L male mice were divided into four groups: sham, I/R, I/R + HCH and I/R + N2/O2 groups. Assessment of animals happened in 'blind' matter. I/R was induced by occlusion of middle cerebral artery for one hour). After one hour, filament was withdrawn, which induced reperfusion. Hydrogen treated I/R animals inhaled mix of 66.7% H2 balanced with O2 for 90 minutes, starting immediately after initiation of reperfusion. Control animals (N2/O2) inhaled mix in which hydrogen was replaced with N2 for the same time (90 minutes). The brain injury, such as brain infarction and development of brain edema, as well as neurobehavioral deficits were determined 23 hours after reperfusion. Effect of HCH on microglia activation in the ischemic penumbra was investigated by immunostaining also 23 hours after reperfusion. mRNA expression of inflammation related genes was detected by PCR. Our results showed that HCH attenuated brain injury and consequently reduced neurological dysfunction after I/R. Furthermore, we demonstrated that HCH directed microglia polarization towards anti-inflammatory M2 polarization. This study indicates hydrogen may exert neuroprotective effects by inhibiting the microglial activation and regulating microglial polarization. This study was conducted in agreement with the Animal Care and Use Committee (IACUC) and Institutional Animal Care guidelines regulation (Shanghai Jiao Tong University, China (approval No. A2015-011) in November 2015.