title: Walnuts (seeds of Juglandis sinensis L.) protect human epidermal keratinocytes against UVB-induced mitochondria-mediated apoptosis through upregulation of ROS elimination pathways.
abstract: OBJECTIVE
  Ultraviolet (UV) light from sunlight is an important environmental factor causing hazardous health effects, including various skin disorders. UV irradiation downregulates reactive oxygen species (ROS) elimination pathways, thereby promoting the production of ROS, which are implicated in mitochondria-mediated apoptosis. Walnuts, the seeds of Juglandis sinensis L., are a highly nutritious food and have been shown to have a number of pharmacological activities. To our knowledge, no study on the protective effects of walnuts on human epidermal keratinocytes has been reported previously. Here, we investigated the protective effects of walnuts against UVB (50 mJ/cm(2)) -induced mitochondria-mediated apoptosis.
  
  
  RESULTS
  Walnuts significantly and dose-dependently reduced UVB-induced apoptotic toxicity by lactate dehydrogenase assay kit. Walnuts decreased mitochondrial dysfunction, B-cell lymphoma 2 (Bcl-2)-associated X (Bax) protein levels, and cytochrome c release from mitochondria, while increasing Bcl-2 protein levels using immunofluorescence, Western blot, or kit analysis. Moreover, walnuts inhibited caspase-3 activity, indicating an inhibition of the apoptotic cascade, and induced the expression of heme oxygenase and NAD(P)H dehydrogenase via NF-E2-related factor-2 activation using immunofluorescence or Western blot analysis.
  
  
  CONCLUSIONS
  Together, these results demonstrate that walnuts can protect human epidermal keratinocytes against UVB-induced mitochondria-mediated apoptosis by regulating ROS elimination pathways.
authors.affiliation: Department of Life and Nanopharmaceutical Science, College of Pharmacy, Kyung Hee University, Seoul, Republic of Korea.
authors.forename: G
authors.initials: G
authors.lastname: Park
authors.forename: H G
authors.initials: HG
authors.lastname: Kim
authors.forename: S-P
authors.initials: SP
authors.lastname: Hong
authors.forename: S Y
authors.initials: SY
authors.lastname: Kim
authors.forename: M S
authors.initials: MS
authors.lastname: Oh
mesh_terms: D017209:Apoptosis / Q000187:drug effects* / Q000528:radiation effects; D015153:Blotting, Western; D053148:Caspase 3 / Q000378:metabolism; D002460:Cell Line; D045304:Cytochromes c / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004817:Epidermis / Q000187:drug effects / Q000528:radiation effects; D005455:Fluorescent Antibody Technique; D006801:Humans; D031324:Juglans / Q000737:chemistry*; D015603:Keratinocytes / Q000187:drug effects* / Q000473:pathology / Q000528:radiation effects; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008928:Mitochondria / Q000187:drug effects / Q000473:pathology / Q000528:radiation effects; D010936:Plant Extracts / Q000008:administration & dosage / Q000494:pharmacology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D012639:Seeds; D014466:Ultraviolet Rays / Q000009:adverse effects; D015854:Up-Regulation / Q000187:drug effects; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D010936:Plant Extracts; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein; D045304:Cytochromes c; D007770:L-Lactate Dehydrogenase; D053148:Caspase 3