title: Astilbin inhibits Th17 cell differentiation and ameliorates imiquimod-induced psoriasis-like skin lesions in BALB/c mice via Jak3/Stat3 signaling pathway.
abstract: The flavonoid astilbin is the major active component extracted from the rhizome of Smilax glabra, which has been widely used in China to treat inflammatory and autoimmune diseases, Psoriasis is a common chronic inflammatory disease in which T helper 17 (Th17) cells play an important role, provoking inflammation. We employed an imiquimod (IMQ)-induced psoriasis-like mouse model to investigate the effect of astilbin in inflammation. Mice were administered 25 to 50mg/kg astilbin. Inflammation of psoriasis-like lesions was assessed by histology, circulating levels of T cells were assessed by flow cytometry and cytokines by bead-based immunoassay. Jak/Stat3 in isolated T cells was assessed by Western blotting and RORγt expression was assessed by RT-PCR. Administration of astilbin ameliorated IMQ-induced keratinocyte proliferation, infiltration of CD3+ cells to psoriatic lesions and ameliorated elevations in circulating CD4+ and CD8+ T cells and inflammatory cytokines (IL-17A, TNF-α, IL-6, IFN-γ and IL-2). In vitro, astilbin inhibited Th17 cell differentiation and IL-17 secretion of isolated T cells, and inhibited Jak/Stat3 signaling in Th17 cells, while up-regulating Stat3 inhibitor SCOSE3 expression in psoriatic lesions. Thus, astilbin likely alleviates psoriasis-like skin lesions by inhibiting Th17 related inflammation. Astilbin represents as an interesting candidate drug for immunoregulation of psoriasis.
authors.affiliation: Beijing University of Chinese Medicine, Beijing 100029, China.
authors.forename: Ting-Ting
authors.initials: TT
authors.lastname: Di
authors.affiliation: Capital Medical University, Beijing 100069, China.
authors.forename: Zhi-Tong
authors.initials: ZT
authors.lastname: Ruan
authors.affiliation: Beijing Hospital of Traditional Chinese Medicine, affiliated with Capital Medical University, Beijing Institute of Traditional Chinese Medicine, Beijing 100010, China.
authors.forename: Jing-Xia
authors.initials: JX
authors.lastname: Zhao
authors.affiliation: Beijing Hospital of Traditional Chinese Medicine, affiliated with Capital Medical University, Beijing Institute of Traditional Chinese Medicine, Beijing 100010, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Beijing Hospital of Traditional Chinese Medicine, affiliated with Capital Medical University, Beijing Institute of Traditional Chinese Medicine, Beijing 100010, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Liu
authors.affiliation: Capital Medical University, Beijing 100069, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Beijing Hospital of Traditional Chinese Medicine, affiliated with Capital Medical University, Beijing Institute of Traditional Chinese Medicine, Beijing 100010, China. Electronic address: liping61871@sina.com.
authors.forename: Ping
authors.initials: P
authors.lastname: Li
mesh_terms: D000634:Aminoquinolines; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D002454:Cell Differentiation / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D044948:Flavonols / Q000494:pharmacology* / Q000627:therapeutic use*; D000077271:Imiquimod; D007155:Immunologic Factors / Q000494:pharmacology* / Q000627:therapeutic use*; D020381:Interleukin-17 / Q000276:immunology; D053616:Janus Kinase 3 / Q000276:immunology; D015603:Keratinocytes / Q000187:drug effects / Q000276:immunology / Q000502:physiology; D008297:Male; D008807:Mice, Inbred BALB C; D011565:Psoriasis / Q000139:chemically induced / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D050796:STAT3 Transcription Factor / Q000276:immunology; D015398:Signal Transduction / Q000187:drug effects; D012867:Skin / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D058504:Th17 Cells / Q000187:drug effects / Q000276:immunology / Q000502:physiology
chemical_list: D000634:Aminoquinolines; D000893:Anti-Inflammatory Agents; D044948:Flavonols; D007155:Immunologic Factors; D020381:Interleukin-17; D050796:STAT3 Transcription Factor; C494087:Stat3 protein, mouse; C099069:astilbin; C507935:Jak3 protein, mouse; D053616:Janus Kinase 3; D000077271:Imiquimod
keywords: Astilbin; IL-17; Imiquimod; Inflammation; Psoriasis; Th17