Vitamin D protects keratinocytes from apoptosis induced by osmotic shock, oxidative stress, and tumor necrosis factor.

摘要: Calcitriol, the hormonal form of vitamin D, inhibited caspase-3-like activation in HaCaT keratinocytes exposed to hyperosmotic and oxidative stresses, heat shock, inflammatory cytokine TNF. The hormone also protected cells from caspase-independent cell death induced by stresses. protection against stress is not affected inhibitors EGF receptor, ERK or PI13 kinase pathways, neither it due reduced activity proapoptotic p38 MAP kinase. These results are accordance with previous vivo findings that D protects epidermal apoptosis UV radiation chemotherapy.