Honokiol protects skin cells against inflammation, collagenolysis, apoptosis, and senescence caused by cigarette smoke damage. (22nd February 2017)

• Record Type: Journal Article
• Authors: Costa, Adilson; Facchini, Gustavo; Pinheiro, Ana Lúcia T. A.; da Silva, Michelle S.; Bonner, Michael Y.; Arbiser, Jack; Eberlin, Samara
• Is Part Of: International journal of dermatology. Volume 56:Number 7(2017)
• Page Start: 754
• Page End: 761
• Publication Date: 2017-02-22
• Subjects: Dermatology -- Periodicals; 616.5
• DOI: 10.1111/ijd.13569
• Languages: English
• ISSNs: 0011-9059

Abstract

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‐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.