Kinase

MAPK/ERK pathway

Cell biology

Eriodictyol

Luteolin

Molecular biology

Biology

Reactive oxygen species

p38 mitogen-activated protein kinases

Signal transduction

Biochemistry

Protein kinase A

Phosphorylation

Genetics

Photoaging

Antioxidant

Matrix metalloproteinase

Chemistry

Quercetin

Journal of Photochemistry and Photobiology B Biology

Solar UVA irradiation-generated reactive oxygen species (ROS) induces the expression of matrix metalloproteinase 1 (MMP-1), leading to photoaging, however the molecular mechanism remains unclear. In the present study, we found that eriodictyol remarkably reduces UVA-mediated ROS generation and protects the skin cells from oxidative damage and the ensuing cell death. Moreover eriodictyol pretreatment significantly down-regulates the UVA-induced MMP-1 expression, and lowers the inflammatory responses within the skin cells. Pretreatment with eriodictyol upregulates the expression of tissue inhibitory metalloproteinase 1 (TIMP-1) and collagen-I (COL-1) at the transcriptional level in a dose-dependent manner. UVA-induced phosphorylation levels of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and p38 leading to increased MMP-1 expression are significantly reduced in eriodictyol-treated skin cells. In addition, eriodictyol pretreatment significantly suppresses inflammatory cytokines and inhibits the activation of MAPK signaling cascades in skin cells. Taken together, our results demonstrate that eriodictyol has both potent anti-inflammatory and anti-photoaging effects.

Eriodictyol protects skin cells from UVA irradiation-induced photodamage by inhibition of the MAPK signaling pathway