PMID- 23499868
OWN - NLM
STAT- MEDLINE
DCOM- 20130610
LR  - 20201209
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 269
IP  - 1
DP  - 2013 May 15
TI  - Oleanolic acid acetate inhibits atopic dermatitis and allergic contact dermatitis 
      in a murine model.
PG  - 72-80
LID - S0041-008X(13)00091-4 [pii]
LID - 10.1016/j.taap.2013.03.001 [doi]
AB  - 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-alpha/IFN-gamma-activated human 
      keratinocyte (HaCaT) model. OAA inhibited the expression of cytokines and 
      chemokines through the downregulation of NF-kappaB 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.
CI  - Copyright (c) 2013 Elsevier Inc. All rights reserved.
FAU - Choi, Jin Kyeong
AU  - Choi JK
AD  - CMRI, Department of Pharmacology, School of Medicine, Kyungpook National 
      University, Daegu 700-422, Republic of Korea.
FAU - Oh, Hyun-Mee
AU  - Oh HM
FAU - Lee, Soyoung
AU  - Lee S
FAU - Park, Jin-Woo
AU  - Park JW
FAU - Khang, Dongwoo
AU  - Khang D
FAU - Lee, Seung Woong
AU  - Lee SW
FAU - Lee, Woo Song
AU  - Lee WS
FAU - Rho, Mun-Chual
AU  - Rho MC
FAU - Kim, Sang-Hyun
AU  - Kim SH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130313
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Anti-Allergic Agents)
RN  - 0 (Antigens, Dermatophagoides)
RN  - 0 (Cytokines)
RN  - 0 (Dinitrochlorobenzene)
RN  - 0 (Inflammation Mediators)
RN  - 0 (NF-kappa B)
RN  - 6SMK8R7TGJ (Oleanolic Acid)
SB  - IM
MH  - Administration, Oral
MH  - Animals
MH  - Anti-Allergic Agents/administration & dosage/*pharmacology
MH  - Antigens, Dermatophagoides
MH  - Cell Line
MH  - Cytokines/metabolism
MH  - Dermatitis, Allergic Contact/genetics/immunology/pathology/*prevention & control
MH  - Dermatitis, Atopic/genetics/immunology/pathology/*prevention & control
MH  - Dinitrochlorobenzene
MH  - Disease Models, Animal
MH  - Eosinophils/drug effects/immunology
MH  - Female
MH  - Gene Expression Regulation/drug effects
MH  - Humans
MH  - Inflammation Mediators/metabolism
MH  - Keratinocytes/drug effects/immunology
MH  - Local Lymph Node Assay
MH  - MAP Kinase Signaling System/drug effects
MH  - Mast Cells/drug effects/immunology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - NF-kappa B/metabolism
MH  - Oleanolic Acid/administration & dosage/*pharmacology
MH  - Skin/*drug effects/immunology/pathology
MH  - T-Lymphocytes/drug effects/immunology
MH  - Time Factors
EDAT- 2013/03/19 06:00
MHDA- 2013/06/12 06:00
CRDT- 2013/03/19 06:00
PHST- 2012/11/23 00:00 [received]
PHST- 2013/02/26 00:00 [revised]
PHST- 2013/03/01 00:00 [accepted]
PHST- 2013/03/19 06:00 [entrez]
PHST- 2013/03/19 06:00 [pubmed]
PHST- 2013/06/12 06:00 [medline]
AID - S0041-008X(13)00091-4 [pii]
AID - 10.1016/j.taap.2013.03.001 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2013 May 15;269(1):72-80. doi: 
      10.1016/j.taap.2013.03.001. Epub 2013 Mar 13.