title: Terminalia Chebulanin Attenuates Psoriatic Skin Lesion via Regulation of Heme Oxygenase-1.
abstract: OBJECTIVE
  Psoriasis is one of the most common inflammatory skin disorders, affecting 3% of the general population. Terminalia chebulanin (TC) is a polyphenolic compound that possesses antioxidant and anti-inflammatory activities. The current study was designed to investigate the effect of TC on psoriatic lesions.
  
  
  METHODS
  We examined the protective effect of TC against psoriatic lesions in mice and keratinocyte proliferation in HaCaT cells.
  
  
  RESULTS
  We found that TC exhibited potent anti-psoriatic activities, as evidenced by improvement of erythema and scaling scores, decrease of epidermal, ear and skinfold thickening, decrease of tumor necrosis factor α (TNFα), interleukin (IL)-17A, IL-23 and matrix metalloproteinase (MMP)-9 expression, and decrease of TBARS content and increase of GSH content in IMQ-treated mice, and decrease of keratinocyte proliferation, TNFα, IL-17A and IL-23 expression, and ROS level in M5-treated cells. All those effects induced by TC were inhibited by zinc protoporphyrin IX (ZnPP), an inhibitor of heme oxygenase (HO)-1, indicating that HO-1 was responsible the anti-psoriatic effect of TC. Moreover, TC inhibited the upregulation of p65 NF-x03BA;B under in vitro psoriatic condition. ZnPP suppressed TC-induced inhibition of p65 NF-x03BA;B expression. Overexpression of p65 NF-x03BA;B significantly suppressed TC-induced decrease of TNFα, IL-17A and IL-23 expression and keratinocyte proliferation, indicating that HO-1-mediated downregulation of NF-x03BA;B was involved in the anti-psoriatic effect of TC.
  
  
  CONCLUSIONS
  The data demonstrate that TC may serve as a potential therapeutic option for psoriatic patients.
authors.affiliation: Department of Dermatology, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.
authors.forename: Jingang
authors.initials: J
authors.lastname: An
authors.forename: Tian
authors.initials: T
authors.lastname: Li
authors.forename: Yingying
authors.initials: Y
authors.lastname: Dong
authors.forename: Zhengxiao
authors.initials: Z
authors.lastname: Li
authors.forename: Jia
authors.initials: J
authors.lastname: Huo
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects; D019938:Cyclin D1 / Q000235:genetics / Q000378:metabolism; D019927:Cyclin E / Q000235:genetics / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D051547:Heme Oxygenase-1 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D047348:Hydrolyzable Tannins / Q000494:pharmacology*; D020381:Interleukin-17 / Q000378:metabolism; D053759:Interleukin-23 / Q000378:metabolism; D015603:Keratinocytes / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D008807:Mice, Inbred BALB C; D008517:Phytotherapy; D011524:Protoporphyrins / Q000494:pharmacology; D011565:Psoriasis / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012867:Skin / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D029766:Terminalia / Q000737:chemistry*; D051996:Transcription Factor RelA / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D019927:Cyclin E; D004791:Enzyme Inhibitors; D047348:Hydrolyzable Tannins; D020381:Interleukin-17; D053759:Interleukin-23; D011524:Protoporphyrins; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; C000608100:chebulanin; D019938:Cyclin D1; C017803:zinc protoporphyrin; D051547:Heme Oxygenase-1; D020780:Matrix Metalloproteinase 9