分子状水素はNrf2シグナル活性化を介してヒトメラノサイトを酸化ストレスから保護する
This study examined the effects of molecular hydrogen (H2) on human melanocytes subjected to oxidative stress, with relevance to vitiligo pathogenesis. In both vitiligo tissue specimens and hydrogen peroxide-exposed melanocytes in vitro, H2 reduced intracellular reactive oxygen species accumulation and malondialdehyde levels in a concentration- and time-dependent fashion, while simultaneously enhancing antioxidant enzyme activity. H2 also reversed hydrogen peroxide-induced apoptosis and mitochondrial dysfunction in normal and vitiligo-derived melanocytes. Mechanistically, H2 promoted Nrf2 signaling activation, and genetic knockdown of Nrf2 abolished the cytoprotective effects of H2. Additionally, H2 upregulated β-catenin in stressed melanocytes, and the Wnt/β-catenin pathway was identified as an upstream regulator of H2-induced Nrf2 activation. These findings suggest that H2 may exert protective effects in melanocytes through a Wnt/β-catenin–Nrf2 axis.
H2 activates Nrf2 signaling through the Wnt/β-catenin pathway, thereby reducing intracellular ROS accumulation, lipid peroxidation, and apoptosis while preserving mitochondrial integrity in melanocytes under oxidative stress.
This is basic research at the cellular or molecular level. For human application, inhalation is the most promising delivery route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration devices are not recommended).
See also:
https://h2-papers.org/en/papers/32234461