@Article{ecn.2015.0364,
AUTHOR = {Abdullah Alyoussef},
TITLE = {Arjunolic acid protects against DNCB-induced atopic dermatitis-like symptoms in mice by restoring a normal cytokine balance},
JOURNAL = {European Cytokine Network},
VOLUME = {26},
YEAR = {2015},
NUMBER = {2},
PAGES = {38--45},
URL = {http://www.techscience.com/ECN/v26n2/65549},
ISSN = {1952-4005},
ABSTRACT = {Purpose: Atopic dermatitis (AD) is a chronically relapsing, pruritic, eczematous skin disorder accompanying
allergic inflammation. AD is triggered by oxidative stress and immune imbalance. The effect of oral
arjunolic acid (AA) on 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis in mice was investigated. Methods:
Repeated epicutaneous application of DNCB to the ear and shaved dorsal skin of mice was performed to induce
AD-like symptoms and skin lesions: 250mg/kg AA was given orally for three weeks to assess its anti-pruritic effects.
Serum levels of tumor necrosis factor (TNF)-α, interleukin (IL)-4, IL-6, IL-10, immunoglobulin (Ig)E and caspase-3
were assessed by ELISA. Results: We found that AA alleviated DNCB-induced AD-like symptoms as quantified by
skin lesions, dermatitis score, ear thickness and scratching behavior. Levels of reactive oxygen species in the AA
group were significantly inhibited compared with those in the DNCB group. In parallel, AA blocked a DNCB-induced
reduction in serum levels of IL-4 and IL-10 associated with an attenuation of DNCB-induced increases in
serum TNF-α, IL-6, IgE and caspase-3. Conclusions: The results indicate that AA suppresses DNCB-induced AD
in mice via redox balance and immune modulation, and could be a safe clinical treatment for AD.},
DOI = {10.1684/ecn.2015.0364}
}