title: Ethanol extracts of Sanguisorba officinalis L. suppress TNF-α/IFN-γ-induced pro-inflammatory chemokine production in HaCaT cells.
abstract: BACKGROUND
  Sanguisorba officinalis L. (SOL) is a perennial plant widely distributed in Asia, its roots are well-known as a traditional herbal medicine to treat burns, chronic intestinal infections, scalds, and inflammation in Korea. Also, the roots of SOL are used for treatment of many types of allergic skin diseases, including urticarial, eczema, and allergic dermatitis.
  
  
  OBJECTIVE
  In this study we investigated the underlying mechanism of anti-inflammatory effect of an ethanol extract of SOL roots (ESOL).
  
  
  METHODS
  The ability of ESOL to inhibit inflammatory skin disorder was tested in human keratinocyte HaCaT cells.
  
  
  METHODS
  Viability test using MTT assay were used to determine non-cytotoxic concentrations of ESOL on HaCaT cells. ESOL-mediated inhibition of the tumor necrosis factor (TNF)-α/interferon (IFN)-γ-induced production of pro-inflammatory chemokines-such as macrophage-derived chemokine (MDC), regulated on activation, normal T-cell expressed and secreted (RANTES), interleukin (IL)-8, and thymus and activation regulated chemokine (TARC)-at the mRNA level was determined by real-time reverse transcription-polymerase chain reaction (RT-PCR). The ability of ESOL to reduce the expression of pro-inflammatory marker proteins was evaluated by Western blot analysis and immunocytochemistry.
  
  
  RESULTS
  ESOL reduced the production of MDC, RANTES, IL-8, and TARC in HaCaT cells stimulated with TNF-α/IFN-γ at both protein and mRNA levels. ESOL also suppressed the phosphorylation of signal transducer and activator of transcription (STAT)-1, extracellular signal-regulated kinase (ERK), and inhibited both nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha (IκB-α) degradation and the nuclear translocation of NF-κB/p65. ESOL exerts anti-inflammatory effects by suppressing the expression of TNF-α/IFN-γ-stimulated chemokines and pro-inflammatory molecules via a blockade NF-κB, STAT-1, and ERK activation.
  
  
  CONCLUSIONS
  Our results suggest the preventive potential of ESOL as a herbal medicine for the treatment of inflammatory skin diseases.
authors.affiliation: Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu, 701-300, Republic of Korea.
authors.forename: Ju-Hye
authors.initials: JH
authors.lastname: Yang
authors.affiliation: Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu, 701-300, Republic of Korea.
authors.forename: Youn-Hwan
authors.initials: YH
authors.lastname: Hwang
authors.affiliation: Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu, 701-300, Republic of Korea.
authors.forename: Min-Jung
authors.initials: MJ
authors.lastname: Gu
authors.affiliation: Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu, 701-300, Republic of Korea. Electronic address: wkcho@kiom.re.kr.
authors.forename: Won-Kyung
authors.initials: WK
authors.lastname: Cho
authors.affiliation: Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu, 701-300, Republic of Korea. Electronic address: jyma@kiom.re.kr.
authors.forename: Jin Yeul
authors.initials: JY
authors.lastname: Ma
mesh_terms: D002460:Cell Line; D054414:Chemokine CCL17 / Q000378:metabolism; D054422:Chemokine CCL22 / Q000378:metabolism; D018946:Chemokine CCL5 / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism*; D003876:Dermatitis, Atopic / Q000188:drug therapy; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D006801:Humans; D020672:I-kappa B Proteins / Q000378:metabolism; D007249:Inflammation / Q000188:drug therapy; D007371:Interferon-gamma / Q000494:pharmacology; D016209:Interleukin-8 / Q000378:metabolism; D015603:Keratinocytes / Q000187:drug effects*; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism; D010766:Phosphorylation; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology*; D050794:STAT1 Transcription Factor / Q000378:metabolism; D031993:Sanguisorba / Q000737:chemistry*; D012867:Skin / Q000187:drug effects; D051996:Transcription Factor RelA / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: C106230:CCL17 protein, human; C483024:CCL5 protein, human; C508606:CXCL8 protein, human; D054414:Chemokine CCL17; D054422:Chemokine CCL22; D018946:Chemokine CCL5; D018925:Chemokines; D020672:I-kappa B Proteins; D016209:Interleukin-8; D016328:NF-kappa B; C000606204:NFKBIA protein, human; D010936:Plant Extracts; C498143:RELA protein, human; D050794:STAT1 Transcription Factor; C494079:STAT1 protein, human; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D000072000:NF-KappaB Inhibitor alpha; D007371:Interferon-gamma; D048049:Extracellular Signal-Regulated MAP Kinases
keywords: Anti-inflammation; Chemokine; HaCaT; Keratinocytes; NF-κB/p65; Sanguisorba officinalis L.