title: Oleanolic acid acetate inhibits atopic dermatitis and allergic contact dermatitis in a murine model.
abstract: Atopic dermatitis (AD) and allergic contact dermatitis (ACD) are common allergic and inflammatory skin diseases caused by a combination of eczema, scratching, pruritus, and cutaneous sensitization with allergens. This paper examines whether oleanolic acid acetate (OAA) modulates AD and ACD symptoms by using an existing AD model based on the repeated local exposure of mite extract (Dermatophagoides farinae extract, DFE) and 2,4-dinitrochlorobenzene to the ears of BALB/c mice. In addition, the paper uses a 2,4-dinitrofluorobenzene-sensitized local lymph node assay (LLNA) for the ACD model. The oral administration of OAA over a four-week period attenuated AD symptoms in terms of decreased skin lesions, epidermal thickness, the infiltration of immune cells (CD4⁺ cells, eosinophils, and mast cells), and serum IgE, IgG2a, and histamine levels. The gene expression of Th1, Th2, Th17, and Th22 cytokines was reduced by OAA in the lymph node and ear tissue, and the LLNA verified that OAA suppressed ACD. The oral administration of OAA over a three-day period attenuated ACD symptoms in terms of ear thickness, lymphocyte proliferation, and serum IgG2a levels. The gene expression of Th1, Th2, and Th17 cytokines was reduced by OAA in the thymus and ear tissue. Finally, to define the underlying mechanism, this paper uses a TNF-α/IFN-γ-activated human keratinocyte (HaCaT) model. OAA inhibited the expression of cytokines and chemokines through the downregulation of NF-κB and MAPKs in HaCaT cells. Taken together, the results indicate that OAA inhibited AD and ACD symptoms, suggesting that OAA may be effective in treating allergic skin disorders.
authors.affiliation: CMRI, Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 700-422, Republic of Korea.
authors.forename: Jin Kyeong
authors.initials: JK
authors.lastname: Choi
authors.forename: Hyun-Mee
authors.initials: HM
authors.lastname: Oh
authors.forename: Soyoung
authors.initials: S
authors.lastname: Lee
authors.forename: Jin-Woo
authors.initials: JW
authors.lastname: Park
authors.forename: Dongwoo
authors.initials: D
authors.lastname: Khang
authors.forename: Seung Woong
authors.initials: SW
authors.lastname: Lee
authors.forename: Woo Song
authors.initials: WS
authors.lastname: Lee
authors.forename: Mun-Chual
authors.initials: MC
authors.lastname: Rho
authors.forename: Sang-Hyun
authors.initials: SH
authors.lastname: Kim
mesh_terms: D000284:Administration, Oral; D000818:Animals; D018926:Anti-Allergic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D039741:Antigens, Dermatophagoides; D002460:Cell Line; D016207:Cytokines / Q000378:metabolism; D017449:Dermatitis, Allergic Contact / Q000235:genetics / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D003876:Dermatitis, Atopic / Q000235:genetics / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D004137:Dinitrochlorobenzene; D004195:Disease Models, Animal; D004804:Eosinophils / Q000187:drug effects / Q000276:immunology; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D015603:Keratinocytes / Q000187:drug effects / Q000276:immunology; D023441:Local Lymph Node Assay; D020935:MAP Kinase Signaling System / Q000187:drug effects; D008407:Mast Cells / Q000187:drug effects / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D016328:NF-kappa B / Q000378:metabolism; D009828:Oleanolic Acid / Q000008:administration & dosage / Q000494:pharmacology*; D012867:Skin / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology; D013997:Time Factors
chemical_list: D018926:Anti-Allergic Agents; D039741:Antigens, Dermatophagoides; D016207:Cytokines; D004137:Dinitrochlorobenzene; D018836:Inflammation Mediators; D016328:NF-kappa B; D009828:Oleanolic Acid