Hydrogen ameliorates oxidative stress via PI3K-Akt signaling pathway in UVB-induced HaCaT cells

Abstract

Chronic ultraviolet (UV) exposure-induced oxidative stress is associated with the pathogenesis of skin damage. However, the nuclear factor erythroid-2-related factor 2 (Nrf2) pathway is a critical factor in protecting cells against UVB-induced injury through inhibiting oxidative stress. Furthermore, Nrf2 activation requires the involvement of the phosphoinositide-3 kinase (PI3K)/protein kinase B (AKT) pathway, which has a major role in survival of various cell types. Molecular hydrogen exerts protective effects on UV-induced injury, but the underlying mechanisms have remained elusive. The present study assessed the protective effects of hydrogen against oxidative stress-induced injury caused by UVB irradiation and investigated the molecular mechanisms. In vitro, UVB-induced HaCaT cells were collected for the detection of reactive oxygen species, 8-iso-prostaglandin F2α, malondialdehyde via fluorescence spectrometry and ELISA; cell activity and cytotoxicity by MTT and lactate dehydrogenase assays, respectively. Additionally, the expression level of PI3K, Akt, Nrf2 and heme oxygenase-1 (HO-1) were investigated using western blot, etc. All of the results indicated that hydrogen decreased the levels of reactive oxygen species, 8-iso-prostaglandin F2α and malondialdehyde, and promoted the UVB exposure-induced expression of PI3K, Akt, Nrf2 and heme oxygenase-1 in HaCaT cells. Of note, PI3K inhibition partially reversed the effects of hydrogen on UVB-induced HaCaT cells. Therefore, hydrogen effectively protects cells from UVB radiation-induced oxidative stress by inhibiting Nrf2/HO-1 activation through the PI3K/Akt signaling pathway.