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Honokiol protects skin cells against inflammation, collagenolysis, apoptosis, and senescence caused by cigarette smoke damage
Author(s) -
Costa Adilson,
Facchini Gustavo,
Pinheiro Ana Lúcia T. A.,
Silva Michelle S.,
Bonner Michael Y.,
Arbiser Jack,
Eberlin Samara
Publication year - 2017
Publication title -
international journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.677
H-Index - 93
eISSN - 1365-4632
pISSN - 0011-9059
DOI - 10.1111/ijd.13569
Subject(s) - hacat , honokiol , apoptosis , inflammation , senescence , medicine , smoke , andrology , cigarette smoke , pharmacology , in vitro , immunology , chemistry , biochemistry , organic chemistry , environmental health
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 ‐1 α 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 μ m reduced IL ‐1 α production by 3.4 folds ( P < 0.05) and at 10 and 20 μ m 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 μ m , 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.