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Kaempferol-3-O-rutinoside from Afgekia mahidoliae promotes keratinocyte migration through FAK and Rac1 activation

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Abstract

The restoration of the epidermal epithelium through re-epithelialization is a critical process in wound healing. Directed keratinocyte migration to the wound is required, and the retardation of this process may result in a chronic, non-healing wound. The present study contributes to research aiming to identify promising compounds that promote wound healing using a human keratinocyte model. The effects of three kaempferol glycosides from an Afgekia mahidoliae leaf extract, kaempferol-3-O-arabinoside, kaempferol-3-O-glucoside, and kaempferol-3-O-rutinoside, on keratinocyte migration were determined. Interestingly, kaempferol-3-O-rutinoside exhibited a pronounced effect on wound closure in comparison to the parental kaempferol and other glycosides. The mechanism by which kaempferol-3-O-rutinoside enhances cell migration involves the induction of filopodia and lamellipodia formation, increased cellular levels of phosphorylated FAK (Tyr 397) and phosphorylated Akt (Ser 473), and up-regulation of active Rac1-GTP. The data obtained in this study may support the development of this compound for use in wound healing therapies.

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Acknowledgments

This research was financially supported by the Ratchadapiseksomphot Endowment Fund of Chulalongkorn University (RES560530157-HR), the 90th Anniversary of Chulalongkorn University Fund (Ratchadapiseksomphot Endowment Fund), and the Unit Cell for Research and Development of Herbs and Natural Products for Dental Application, Chulalongkorn University. We would like to acknowledge Associate Professor Rutt Suttisri, Ph.D. for his help in the isolation process. We also thank the Chulalongkorn University Centenary Academic Development Project for providing the facility used for this research.

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Correspondence to Pithi Chanvorachote or Suchada Sukrong.

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Petpiroon, N., Suktap, C., Pongsamart, S. et al. Kaempferol-3-O-rutinoside from Afgekia mahidoliae promotes keratinocyte migration through FAK and Rac1 activation. J Nat Med 69, 340–348 (2015). https://doi.org/10.1007/s11418-015-0899-3

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  • DOI: https://doi.org/10.1007/s11418-015-0899-3

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