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.
本文討論了氫氣在急性缺血性中風和再灌注損傷中的潛在神經保護作用。首先強調了美國中風的患病率和影響，儘管治療方法取得了進步。
該文章強調，缺血事件後血流恢復後，細胞損傷仍然存在。目前的干預措施尚未確定單一可行的分子來解決中風引起的損傷所涉及的複雜病理過程。
氫因其具有廣泛的可用性、通過細胞膜快速擴散、惰性以及與侵蝕性活性氧(ROS) 反應的能力等特性，作為一種潛在的神經保護劑而受到關注。
再灌注損傷，被稱為“氧悖論”，涉及缺血組織再灌注後活性氧的過量產生。ROS，包括羥基、超氧化物和過氧亞硝酸鹽，在細胞死亡和細胞凋亡途徑中發揮作用。
氫具有猝滅能力，可減少脂質過氧化、防止DNA 氧化並減少谷氨酸毒性引起的神經元死亡。它還調節細胞對氧化應激、炎症和細胞凋亡途徑的反應。
本文討論了氫增強線粒體自噬、增加抗氧化酶表達和發揮抗炎作用的機制。研究表明，氫氣在缺血動物模型以及通過吸入或水給藥的人體研究中具有積極作用。
氫氣暴露的安全性已得到證實，並且有望在血運重建過程中作為神經保護劑。文章最後提倡進行更大規模的隨機雙盲研究，以進一步探索氫氣在急性中風治療中的潛在作用。