Honokiol protects skin cells against inflammation, collagenolysis, apoptosis, and senescence caused by cigarette smoke damage.

Abstract

BACKGROUND Pollution, especially cigarette smoke, is a major cause of skin damage. OBJECTIVES To assess the effects of the small molecule polyphenol, honokiol, on reversing cigarette smoke-induced damage in vitro to relevant skin cells. METHODS Keratinocytes (HaCat) cultures were exposed to cigarette smoke and, after 48 hours, IL-1α and IL-8 were measured in cell supernatants. Moreover, TIMP-2 production, apoptosis rate, and senescence β-galactosidase expression were evaluated in primary human foreskin fibroblasts (HFF-1) cultures. RESULTS Honokiol at 10 μm reduced IL-1α production by 3.4 folds (P < 0.05) and at 10 and 20 μm reduced IL-8 by 23.9% and 53.1% (P < 0.001), respectively, in HaCat keratinocytes. In HFF-1, honokiol restored TIMP-2 production by 96.9% and 91.9% (P < 0.001), respectively, at 10 and 20 μm, as well as reduced apoptosis by 47.1% (P < 0.001) and 41.3% (P < 0.01), respectively. Finally, honokiol reduced senescence-associated β-galactosidase expression in HFF-1. CONCLUSION Honokiol protects both HFF-1 and HaCat against cigarette smoke-induced inflammation, collagenolysis, apoptosis, and senescence.

DOI: 10.1111/ijd.13569

Cite this paper

@article{Costa2017HonokiolPS, title={Honokiol protects skin cells against inflammation, collagenolysis, apoptosis, and senescence caused by cigarette smoke damage.}, author={Adilson Rodrigues da Costa and Gustavo Facchini and Ana L{\'u}cia T A Pinheiro and Michelle Soares Josino da Silva and Michael Yi Bonner and Jack L. Arbiser and Samara Eberlin}, journal={International journal of dermatology}, year={2017}, volume={56 7}, pages={754-761} }