title: Paeoniflorin inhibits imiquimod-induced psoriasis in mice by regulating Th17 cell response and cytokine secretion.
abstract: Paeoniflorin (PF) is the main active ingredients of radix paeoniae rubra and radix paeoniae alba, which are used widely in Traditional Chinese Medicine. This study aimed to assess the capacity of PF to inhibit imiquimod (IMQ)-induced psoriasis. Mice treated with IMQ were divided into four groups and administered 240mg/kg/day or 120mg/kg/day of PF, 1mg/kg/day of methotrexate (MTX), or normal saline intragastrically. Weight-matched mice treated with vaseline were used as controls. Morphology, structural features, keratinocyte proliferation and differentiation, inflammatory cell infiltration, levels of Th1/Th2/Th17/Treg cytokine mRNA, and phosphorylation of Th17 differentiation-related proteins were assessed. Mouse spleen cells were incubated under Th17 polarizing conditions, then with PF (2, 20, and 200μg/ml) and cell viability, Th17 differentiation, and Th17 cytokines and the orphan nuclear receptor (RORγt) mRNA levels were assessed. PF alleviated IMQ-induced keratinocyte proliferation and inflammatory cell infiltration, and reduced mRNA levels of Th17 cytokines at day 4 and phosphorylation of Th17 differentiation-related proteins. However, 2, 20, or 200μg/ml PF did not affect spleen cell viability, and 2 and 20μg/ml PF reduced IL-17 secretion under Th17 polarizing conditions. Finally, 2 and 20μg/ml PF inhibited mRNA expression of Th17 cytokines and phosphorylation of Stat3 in spleen cells under Th17 polarizing conditions. These results suggest that PF inhibits IMQ-induced psoriasis by regulating Th17 cell response and cytokine secretion via phosphorylation of Stat3.
authors.affiliation: Beijing Key Laboratory of Clinic and Basic Research with Traditional Chinese Medicine on Psoriasis, Beijing Institute of Traditional Chinese Medicine, Beijing 100010, China; Beijing Hospital of Traditional Chinese Medicine, Affiliated with Capital Medical University, Beijing 100010, China.
authors.forename: Jingxia
authors.initials: J
authors.lastname: Zhao
authors.affiliation: Beijing Key Laboratory of Clinic and Basic Research with Traditional Chinese Medicine on Psoriasis, Beijing Institute of Traditional Chinese Medicine, Beijing 100010, China.
authors.forename: Tingting
authors.initials: T
authors.lastname: Di
authors.affiliation: Beijing Key Laboratory of Clinic and Basic Research with Traditional Chinese Medicine on Psoriasis, Beijing Institute of Traditional Chinese Medicine, Beijing 100010, China; Beijing Hospital of Traditional Chinese Medicine, Affiliated with Capital Medical University, Beijing 100010, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Beijing Key Laboratory of Clinic and Basic Research with Traditional Chinese Medicine on Psoriasis, Beijing Institute of Traditional Chinese Medicine, Beijing 100010, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Beijing Key Laboratory of Clinic and Basic Research with Traditional Chinese Medicine on Psoriasis, Beijing Institute of Traditional Chinese Medicine, Beijing 100010, China; Beijing Hospital of Traditional Chinese Medicine, Affiliated with Capital Medical University, Beijing 100010, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Liu
authors.affiliation: Beijing Key Laboratory of Clinic and Basic Research with Traditional Chinese Medicine on Psoriasis, Beijing Institute of Traditional Chinese Medicine, Beijing 100010, China.
authors.forename: Daiying
authors.initials: D
authors.lastname: Liang
authors.affiliation: Beijing Key Laboratory of Clinic and Basic Research with Traditional Chinese Medicine on Psoriasis, Beijing Institute of Traditional Chinese Medicine, Beijing 100010, China; Beijing Hospital of Traditional Chinese Medicine, Affiliated with Capital Medical University, Beijing 100010, China. Electronic address: liping08184@sina.com.
authors.forename: Ping
authors.initials: P
authors.lastname: Li
mesh_terms: D000634:Aminoquinolines / Q000494:pharmacology*; D000818:Animals; D002454:Cell Differentiation / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000187:drug effects; D005960:Glucosides / Q000494:pharmacology* / Q000627:therapeutic use; D000077271:Imiquimod; D015603:Keratinocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D051379:Mice; D039821:Monoterpenes / Q000494:pharmacology* / Q000627:therapeutic use; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics; D010766:Phosphorylation / Q000187:drug effects; D011565:Psoriasis / Q000139:chemically induced / Q000188:drug therapy* / Q000276:immunology* / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000378:metabolism; D012867:Skin / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D058504:Th17 Cells / Q000166:cytology / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism*; D006027:Glycosides
chemical_list: D000634:Aminoquinolines; D016207:Cytokines; D005960:Glucosides; D000077271:Imiquimod; D039821:Monoterpenes; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D012333:RNA, Messenger; D050796:STAT3 Transcription Factor; C015423:peoniflorin; D006027:Glycosides
keywords: Cytokine secretion; Imiquimod; Paeoniflorin; Psoriasis; Th17