Steroidal agent is a standard clinical treatment of
atopic dermatitis; however, have serious side effects.
Artesunate is reported to exhibit anti-inflammatory properties although its effect on
atopic eczema remains unknown. We investigated the
therapeutic effects and possible mechanism of systemic
artesunate on
DNCB-induced
atopic dermatitis in a BALB/c mouse model. To ascertain
artesunate (5 and 10 mg/kg) efficacy, skin
dermatitis severity and ear, spleen, and lymph node weight were evaluated. Skin tissue
mRNA and
protein expression and serum
cytokine levels were examined.
Artesunate significantly improved
atopic dermatitis symptoms, decreasing the
dermatitis score, ear weight difference, spleen weight, and lymph node weight compared with those following
DNCB treatment.
Artesunate reduced ear and skin epidermal thickness and mast cell infiltration, as determined using
hematoxylin-
eosin and
toluidine blue staining, respectively. The basal level of
IgE (287.67 ± 70.41 ng/ml) and TNF-α (19.94 ± 3.98 pg/ml) were Significantly elevated by
DNCB (
IgE: 1273.23 ± 176.53 ng/ml; TNF-α: 57.53 ± 3.87 pg/ml), while markedly been suppressed in the treatment group (AS-L:
IgE: 1100.25 ± 135.32 ng/ml; TNF-α: 38.47 ± 3.26 pg/ml; AS-H:
IgE: 459.46 ± 74.75 ng/ml; TNF-α: 24.38 ± 3.85 pg/ml). Among Th17 cell-related factors,
DNCB treatment increased
mRNA expression of
IL-6,
IL-17,
IL-23, STAT3, and ROR-γt, but reduced TGF-β and SOCS 3; While
artesunate reverse these changes. Compared with the model group,
artesunate promoted
SOCS3 protein and significantly inhibited ROR-γt
protein and STAT3 phosphorylation. Thus,
artesunate attenuates
DNCB-induced
atopic dermatitis by inhibiting the release of inflammatory
cytokines and downregulating Th17 cell responses in
atopic dermatitis mice.