Capsiate, one of the major capsaicinoids, is nonpungent and present in sweet pepper. We investigated the effects of
capsiate on the ultraviolet B (UVB)-induced inflammatory response in skin and its molecular mechanisms.
Capsiate-pretreated human keratinocytes inhibited intracellular
reactive oxygen species (ROS), which activate the
mitogen-activated protein kinase and
nuclear factor-kappaB (
NF-kappaB) pathways. Therefore, we determined the effects of
capsiate on these pathways.
Capsiate inhibited UVB-induced
cyclooxygenase-2 (COX-2) expression, extracellular signal-related
kinase 1/2 phosphorylation, nuclear translocation of
NF-kappaB, and the expression of proinflammatory
cytokines and potent angiogenic factors, including vascular endothelial cell
growth factor and
matrix metalloproteinase-2 (MMP-2) and MMP-9. In addition,
capsiate inhibited UVB-induced
epidermal growth factor receptor (EGFR) activation, which reduces the levels of proinflammatory
cytokines and angiogenic factors. We also investigated the photoprotective effects of
capsiate in vivo. Topical treatment with
capsiate significantly decreased UVB-induced skin damage and inhibited the expression of COX-2, proinflammatory
cytokines, and angiogenic factors, including
platelet/endothelial cell adhesion molecule-1 and
intercellular adhesion molecule-1. Inhibition of
Src kinase activity and ROS may inhibit the EGFR activation. Therefore,
capsiate may protect the skin from UVB-induced adverse effects and these results provide a molecular basis for understanding its effects on
inflammation and angiogenesis.