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 in | International journal of dermatology Vol. 56; no. 7; pp. 754 - 761 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Blackwell Publishing Ltd
01.07.2017
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Subjects | |
Online Access | Get full text |
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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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0011-9059 1365-4632 |
DOI: | 10.1111/ijd.13569 |