Literature DB >> 28229451

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

Adilson Costa1, Gustavo Facchini2, Ana Lúcia T A Pinheiro2, Michelle S da Silva2, Michael Y Bonner1, Jack Arbiser1, Samara Eberlin2.   

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.
© 2017 The International Society of Dermatology.

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Year:  2017        PMID: 28229451      PMCID: PMC5464984          DOI: 10.1111/ijd.13569

Source DB:  PubMed          Journal:  Int J Dermatol        ISSN: 0011-9059            Impact factor:   2.736


  90 in total

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