FUTURE NEUROLOGY VOL. 14, NO. 3 | EDITORIAL
This article discusses the potential neuroprotective effects of hydrogen in the context of acute ischemic stroke and reperfusion injury. It begins by highlighting the prevalence and impact of stroke in the United States, despite advancements in treatment.
The article emphasizes that cellular damage persists after blood flow is restored following an ischemic event. Current interventions have not identified a single viable molecule to address the complex pathological processes involved in stroke-induced damage.
Hydrogen has gained interest as a potential neuroprotectant due to its characteristics, including wide availability, rapid diffusion through cell membranes, inert nature, and ability to react with aggressive reactive oxygen species (ROS).
Reperfusion injury, known as the ‘oxygen paradox,’ involves excessive production of ROS following reperfusion of ischemic tissue. ROS, including hydroxyl, superoxide, and peroxynitrite, play roles in cell death and apoptosis pathways.
Hydrogen exhibits quenching capabilities that decrease lipid peroxidation, prevent DNA oxidation, and reduce glutamate toxicity-induced neuronal death. It also modulates cellular responses to oxidative stress, inflammation, and apoptosis pathways.
The article discusses the mechanisms by which hydrogen enhances mitophagy, increases antioxidant enzyme expression, and exerts anti-inflammatory effects. Studies have shown hydrogen’s positive effects in animal models of ischemia, as well as in human studies where it was administered through inhalation or water.
The safety of hydrogen exposure has been demonstrated, and it holds promise as a neuroprotector during revascularization. The article concludes by advocating for larger randomized double-blind studies to further explore hydrogen’s potential role in acute stroke treatment.