title: Inhibitory effect of Patrinia scabiosifolia Link on the development of atopic dermatitis-like lesions in human keratinocytes and NC/Nga mice.
abstract: BACKGROUND
  Atopic dermatitis (AD) is a chronic pruritic and inflammatory disease occurring in skin. Patrinia scabiosifolia Link (PS), a member of the Patrinia genus (Caprifoliaceae family), has traditionally been used in folk medicines to treat various inflammatory diseases such as acute appendicitis, ulcerative colitis, and pelvic inflammation in Korea and other parts of East Asia.
  
  
  OBJECTIVE
  This study investigated the anti-inflammatory effects of PS on AD in vitro and in vivo.
  
  
  METHODS
  Whole PS plants were dried, powdered, and then underwent extraction with DMSO. Both ELISA and western blotting were performed to evaluate cytokine concentration and the expression and activation of filaggrin and signaling proteins. Five-week-old female NC/Nga mice were used as an AD-like mouse model by treating them with 2,4-dinitrochlorobenzene (DNCB).
  
  
  RESULTS
  In human keratinocytic HaCaT cells, PS extract inhibited the production of IL-8, and TARC, which had been increased by TNF-α and IFN-γ. The TNF-α and IFN-γ suppressed filaggrin expression was associated with phosphorylation of JNK1 and JNK2, and NF-κB translocation. PS recovered the inhibition of filaggrin expression induced by TNF-α and IFN-γ by blocking the activation of JNK1/2, and NF-κB by the IFN-γ and TNF-α treatment. The in vivo experiment results showed that, compared to DNCB treatment PS administration reduced thickening of the epidermis and infiltration of inflammatory cells into the dermis. Moreover, the decrease of filaggrin expression due to DNCB treatment was recovered by PS administration. The serum IgE level was decreased by PS treatment. Additionally, secretions of IL-4, IL-5, IL-13, and eotaxin in splenocytes were lower in the PS-treated group than in the DNCB group.
  
  
  CONCLUSIONS
  PS may attenuate the development of AD-like lesions by increasing filaggrin expression and lowering IgE and inflammatory cytokine levels. These results indicate the potential for development of a PS-based drug treatment for AD.
authors.affiliation: Department of Clinical Pathology, Sohae College, Gunsan 54116, Korea; Department of Senior Healthcare, BK21 Plus Program, Graduate School, Eulji University, Daejeon 34824.
authors.forename: Kyung-Jae
authors.initials: KJ
authors.lastname: Cha
authors.affiliation: Department of Clinical Laboratory Science, Wonkwang Health Science University, Iksan 54538; Department of Biomedical Laboratory Science, School of Medicine, Eulji University, Daejeon 34824, Republic of Korea.
authors.forename: Mi Ae
authors.initials: MA
authors.lastname: Im
authors.affiliation: Department of Senior Healthcare, BK21 Plus Program, Graduate School, Eulji University, Daejeon 34824.
authors.forename: Ayoung
authors.initials: A
authors.lastname: Gu
authors.affiliation: Department of Senior Healthcare, BK21 Plus Program, Graduate School, Eulji University, Daejeon 34824.
authors.forename: Da Hye
authors.initials: DH
authors.lastname: Kim
authors.affiliation: Department of Senior Healthcare, BK21 Plus Program, Graduate School, Eulji University, Daejeon 34824.
authors.forename: Daye
authors.initials: D
authors.lastname: Lee
authors.affiliation: Department of Senior Healthcare, BK21 Plus Program, Graduate School, Eulji University, Daejeon 34824.
authors.forename: Jeong Soo
authors.initials: JS
authors.lastname: Lee
authors.affiliation: Department of Clinical Laboratory Science, Wonkwang Health Science University, Iksan 54538. Electronic address: jslee1216@wu.ac.kr.
authors.forename: Ji-Sook
authors.initials: JS
authors.lastname: Lee
authors.affiliation: Department of Senior Healthcare, BK21 Plus Program, Graduate School, Eulji University, Daejeon 34824; Department of Biomedical Laboratory Science, School of Medicine, Eulji University, Daejeon 34824, Republic of Korea. Electronic address: orientree@eulji.ac.kr.
authors.forename: In Sik
authors.initials: IS
authors.lastname: Kim
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D002478:Cells, Cultured; D016207:Cytokines / Q000096:biosynthesis; D003876:Dermatitis, Atopic / Q000188:drug therapy* / Q000473:pathology; D005260:Female; D000091344:Filaggrin Proteins; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D007381:Intermediate Filament Proteins / Q000378:metabolism; D015603:Keratinocytes / Q000187:drug effects*; D048670:MAP Kinase Kinase 4 / Q000378:metabolism; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism; D032405:Patrinia / Q000737:chemistry*; D010936:Plant Extracts / Q000494:pharmacology* / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; C000717249:FLG protein, human; D000091344:Filaggrin Proteins; D007381:Intermediate Filament Proteins; D016328:NF-kappa B; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; D048670:MAP Kinase Kinase 4
keywords: Anti-inflammatory effect; Atopic dermatitis; Filaggrin; Immunoglobulin E; Patrinia scabiosifolia Link