An UVB injury model was established using in vitro cultured HaCaT keratinocytes. Cellular apoptosis, ROS level and inflammatory factor expression were detected to evaluate the protective function of chlorogenic acid.
Key Findings:
Chlorogenic acid at appropriate concentrations markedly reduced ROS accumulation and inhibited apoptosis after UVB irradiation.
Chlorogenic acid downregulated key inflammatory pathway genes and relieved UV-triggered skin inflammatory responses.
Tea-derived chlorogenic acid has great potential to be developed as a natural photoprotective raw material for skincare.