title: Formula PSORI-CM01 inhibits the inflammatory cytokine and chemokine release in keratinocytes via NF-κB expression.
abstract: Psoriasis is a common chronic inflammatory disease in which T-helper 1(Th1) and T-helper 17(Th17) cells play an important role in its pathology. Formula PSORI-CM01 was a novel formulated Chinese medicine used for psoriasis therapy. It had been demonstrated previously that PSORI-CM01 and serum contained Formula PSORI-CM01 (PCM01CS) could improve psoriasis by inhibiting the epithelial hyperplasia, how PSORI-CM01 affects inflammatory cytokine and chemokine in dermis is still unknown. In this study we found PSORI-CM01 pre-treated 3days before IMQ painting could ameliorated IMQ-induced mice skin lesion as PASI score was apparently reduced. Th1 related cytokine IFN-γ and Th17 related cytokine IL-17/IL-22 was used to induce inflammatory models on human keratinocyte cell line HaCaT in vitro, respectively. PCM01CS significantly reduced IFN-γ induced mRNA expression of IL-6, IL-12 and CXCL-10, reduced IL-6 and CXCL-10 release into HaCaT supernatant. 20ng/ml IL-17/IL-22 co-stimulation significantly upregulated expression of IL-6, IL-8 and CCL20 mRNA expression in HaCaT cells, PCM01CS significantly inhibit these cytokines expression both in mRNA and in protein levels. Finally, PCM01CS could obviously inhibit nuclear NF-κB p65 expression which activated by IFN-γ and IL-17/IL-22 stimulation. Thus, our new findings reveal that Formula PSORI-CM01 may possess therapeutic action on psoriasis by inhibiting inflammatory within skin environments.
authors.affiliation: The Second Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Guangdong 510006, China.
authors.forename: Ling
authors.initials: L
authors.lastname: Han
authors.affiliation: The Second Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Guangdong 510006, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Sun
authors.affiliation: Dermatology Department, Guangdong Provincial Hospital of Chinese Medicine, Guangdong 510120, China. Electronic address: luchuanjian888@vip.sina.com.
authors.forename: Chuan-Jian
authors.initials: CJ
authors.lastname: Lu
authors.affiliation: The Second Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Guangdong 510006, China.
authors.forename: Rui-Zhi
authors.initials: RZ
authors.lastname: Zhao
authors.affiliation: The Second Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Guangdong 510006, China.
authors.forename: Yue
authors.initials: Y
authors.lastname: Lu
authors.affiliation: The Second Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Guangdong 510006, China.
authors.forename: Han-Jie
authors.initials: HJ
authors.lastname: Lin
authors.affiliation: The Second Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Guangdong 510006, China. Electronic address: andycarrier@163.com.
authors.forename: Jian-An
authors.initials: JA
authors.lastname: Wei
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D002460:Cell Line; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D004365:Drugs, Chinese Herbal / Q000627:therapeutic use*; D006801:Humans; D015603:Keratinocytes / Q000187:drug effects* / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D011565:Psoriasis / Q000139:chemically induced / Q000188:drug therapy*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012867:Skin / Q000187:drug effects* / Q000473:pathology; D018417:Th1 Cells / Q000187:drug effects* / Q000276:immunology; D058504:Th17 Cells / Q000187:drug effects* / Q000276:immunology; D051996:Transcription Factor RelA / Q000378:metabolism*
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D004365:Drugs, Chinese Herbal; C000601118:PSORI-CM01; C498143:RELA protein, human; D051996:Transcription Factor RelA
keywords: Anti-inflammatory; Chemokines; Cytokines; Keratinocyte; NF-κB; PSORI-CM01