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

Int J Dermatol. 2017 Jul;56(7):754-761. doi: 10.1111/ijd.13569. Epub 2017 Feb 22.

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.

MeSH terms

  • Antioxidants / pharmacology*
  • Apoptosis / drug effects
  • Biphenyl Compounds / pharmacology*
  • Cells, Cultured
  • Cellular Senescence / drug effects
  • Fibroblasts
  • Humans
  • Inflammation / metabolism
  • Interleukin-1alpha / metabolism
  • Interleukin-8 / metabolism
  • Lignans / pharmacology*
  • Tissue Inhibitor of Metalloproteinase-2 / metabolism
  • Tobacco Smoke Pollution / adverse effects*
  • beta-Galactosidase / metabolism

Substances

  • Antioxidants
  • Biphenyl Compounds
  • Interleukin-1alpha
  • Interleukin-8
  • Lignans
  • Tobacco Smoke Pollution
  • honokiol
  • Tissue Inhibitor of Metalloproteinase-2
  • beta-Galactosidase