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

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 cigarett...

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Published inInternational journal of dermatology Vol. 56; no. 7; pp. 754 - 761
Main Authors Costa, Adilson, Facchini, Gustavo, Pinheiro, Ana Lúcia T. A., Silva, Michelle S., Bonner, Michael Y., Arbiser, Jack, Eberlin, Samara
Format Journal Article
LanguageEnglish
Published England Blackwell Publishing Ltd 01.07.2017
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Summary: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.
Bibliography:ObjectType-Article-1
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content type line 23
ISSN:0011-9059
1365-4632
DOI:10.1111/ijd.13569