Myricetin protects keratinocyte damage induced by UV through IκB/NFκb signaling pathway

Summary

Objective

The aim of this study was to evaluate the potential molecular mechanism of myricetin that protecting cells from photodamage.

Methods

Myricetin had broadly chemopreventive effects and anti-inflammatory properties. The effect of myricetin was assessed on HaCaT cells. Cell viability assay was carried out. Reactive oxygen species (ROS) level was measured. The expression of pro-inflammatory factor COX2 was determined by real-time PCR and Western blot. The protein levels of p-IκBa and IκBa were determined by Western blot.

Results

Myricetin attenuated UV-induced keratinocyte death in a dose-dependent manner as determined by cell viability assay. Pretreatment with myricetin also reduced the UV-induced ROS levels. Myricetin suppresses the upregulation of COX2 induced by UV in keratinocyte as demonstrated by real-time PCR and Western blot. Furthermore, signal transduction studies confirmed that myricetin attenuates the upregulation of COX2 induced by UV via suppression of IκB/NFκB pathways.

Conclusion

These results showed that antioxidant property of myricetin can effectively attenuate UV-caused cell damage and suppress the expression of COX2 through the IκB/NFκB signaling pathways. Myricetin had potential protective effects on UV-induced skin cell damages, which might be used in cosmetic and pharmaceutical industries.

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