Abstract Title:

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

Abstract Source:

Int J Dermatol. 2017 Jul ;56(7):754-761. Epub 2017 Feb 22. PMID: 28229451

Abstract Author(s):

Adilson Costa, Gustavo Facchini, Ana Lúcia T A Pinheiro, Michelle S da Silva, Michael Y Bonner, Jack Arbiser, Samara Eberlin

Article Affiliation:

Adilson Costa


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 10μm reduced IL-1α production by 3.4 folds (P<0.05) and at 10 and 20μm 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 20μm, as well as reduced apoptosis by 47.1% (P<0.001) and 41.3% (P<0.01), respectively. Finally, honokiol reduced senescence-associatedβ-galactosidase expression in HFF-1.

CONCLUSION: Honokiol protects both HFF-1 and HaCat against cigarette smoke-induced inflammation, collagenolysis, apoptosis, and senescence.

Study Type : In Vitro Study

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Sayer Ji
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