期刊
BIOMOLECULES & THERAPEUTICS
卷 30, 期 6, 页码 501-509出版社
KOREAN SOC APPLIED PHARMACOLOGY
DOI: 10.4062/biomolther.2022.024
关键词
Atopy; Dermatitis; NJK14047; Immunopharmacology; p38 MAPK
资金
- Basic Research Laboratory Program (BRL) of the Korean National Research Foundation - Korean Ministry of Science, ICT, and Future Planning [NRF-2020R1A4A1016142, NRF-2019R1A2C1005523]
- Basic Science Research Program of the Korean National Research Foundation - Korean Ministry of Science, ICT, and Future Planning [NRF-2020R1A4A1016142, NRF-2019R1A2C1005523]
Atopic dermatitis is a chronic inflammatory skin disorder. Traditional Chinese medicines for AD therapy have been found to suppress MAPKs and NF-.B. This study examined the effect of the p38 MAPK inhibitor NJK14047 on AD-like skin lesions induced in mice and found that it effectively suppressed AD symptoms and reduced cytokine levels.
Atopic dermatitis (AD) is a chronic inflammatory skin disorder. Suppression of MAPKs and NF-.B is implicated as a vital mechanism of action of several traditional Chinese medicines for AD therapy. Although overexpression of MAPK mRNA in the skin tissue has been shown in the AD model, the roles of each MAPK in AD pathogenesis have rarely been studied. This study examined the effect of NJK14047, an inhibitor of p38 MAPKs, on AD-like skin lesions induced in BALB/c mice by sensitization and challenges with 1-chloro-2,4-dinitrobenzene (CDNB) on dorsal skin and ears, respectively. After induction of AD, NJK14047 (2.5 mg/kg) or dexamethasone (10 mg/kg) was administrated for 3 weeks via intraperitoneal injection. Following its administration, NJK14047 suppressed CDNB-induced AD-like symptoms such as skin hypertrophy and suppressed mast cell infiltration into the skin lesions. It also reduced CDNB-induced increase in T(H)2 cytokine (IL-13) and T(H)1 cytokines (interferon-gamma and IL-12A) levels but did not decrease serum IgE level. Furthermore, NJK14047 blocked CDNB-induced lymph node enlargement. These results suggest that NJK14047, a p38 MAPK inhibitor, might be an optimal therapeutic option with unique modes of action for AD treatment.
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