UVB照射HaCaT細胞における水素のPI3K-Aktシグナル経路を介した酸化ストレス軽減効果
UVB irradiation generates oxidative stress implicated in skin cell damage. Using UVB-exposed HaCaT keratinocytes as an in vitro model, this study examined whether molecular hydrogen could counteract the resulting cellular injury. Fluorescence spectrometry and ELISA measurements showed that hydrogen reduced intracellular reactive oxygen species, 8-iso-prostaglandin F2α, and malondialdehyde levels. MTT and lactate dehydrogenase assays confirmed improved cell viability and reduced cytotoxicity. Western blot analysis revealed upregulation of PI3K, Akt, Nrf2, and heme oxygenase-1 (HO-1) following hydrogen exposure. Critically, pharmacological inhibition of PI3K partially abolished these protective effects, indicating that the PI3K/Akt axis is required for hydrogen-driven Nrf2/HO-1 activation and the consequent reduction in oxidative damage under UVB conditions.
Molecular hydrogen activates the PI3K/Akt signaling pathway, which in turn upregulates Nrf2 and HO-1 expression, leading to suppression of ROS generation and lipid peroxidation in UVB-irradiated keratinocytes.
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/29532858