title: Honokiol protects skin cells against inflammation, collagenolysis, apoptosis, and senescence caused by cigarette smoke damage.
abstract: BACKGROUND
  Pollution, especially cigarette smoke, is a major cause of skin damage.
  
  
  OBJECTIVE
  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.
  
  
  CONCLUSIONS
  Honokiol protects both HFF-1 and HaCat against cigarette smoke-induced inflammation, collagenolysis, apoptosis, and senescence.
authors.affiliation: Department of Dermatology, Emory University School of Medicine, Atlanta Veterans Administration Medical Center, Winship Cancer Institute, Atlanta, GA, USA.
authors.forename: Adilson
authors.initials: A
authors.lastname: Costa
authors.affiliation: KOLderma Clinical Trials Institute - Kosmoscience Group, Campinas, SP, Brazil.
authors.forename: Gustavo
authors.initials: G
authors.lastname: Facchini
authors.affiliation: KOLderma Clinical Trials Institute - Kosmoscience Group, Campinas, SP, Brazil.
authors.forename: Ana Lúcia T A
authors.initials: ALTA
authors.lastname: Pinheiro
authors.affiliation: KOLderma Clinical Trials Institute - Kosmoscience Group, Campinas, SP, Brazil.
authors.forename: Michelle S
authors.initials: MS
authors.lastname: da Silva
authors.affiliation: Department of Dermatology, Emory University School of Medicine, Atlanta Veterans Administration Medical Center, Winship Cancer Institute, Atlanta, GA, USA.
authors.forename: Michael Y
authors.initials: MY
authors.lastname: Bonner
authors.affiliation: Department of Dermatology, Emory University School of Medicine, Atlanta Veterans Administration Medical Center, Winship Cancer Institute, Atlanta, GA, USA.
authors.forename: Jack
authors.initials: J
authors.lastname: Arbiser
authors.affiliation: KOLderma Clinical Trials Institute - Kosmoscience Group, Campinas, SP, Brazil.
authors.forename: Samara
authors.initials: S
authors.lastname: Eberlin
mesh_terms: D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D001713:Biphenyl Compounds / Q000494:pharmacology*; D002478:Cells, Cultured; D016922:Cellular Senescence / Q000187:drug effects; D005347:Fibroblasts; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D053582:Interleukin-1alpha / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D017705:Lignans / Q000494:pharmacology*; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000378:metabolism; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*; D001616:beta-Galactosidase / Q000378:metabolism; D000498:Allyl Compounds; D010636:Phenols
chemical_list: D000975:Antioxidants; D001713:Biphenyl Compounds; D053582:Interleukin-1alpha; D016209:Interleukin-8; D017705:Lignans; D019716:Tissue Inhibitor of Metalloproteinase-2; D014028:Tobacco Smoke Pollution; D001616:beta-Galactosidase; C005499:honokiol; D000498:Allyl Compounds; D010636:Phenols