期刊
MOLECULAR MEDICINE REPORTS
卷 24, 期 6, 页码 -出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2021.12467
关键词
atopic dermatitis; Lycopus lucidus Turcz; 2,4-dinitrochlorobenzene; HaCaT; MAPK; NF-kappa B; thymus and activation-regulated chemokine
资金
- National Research Foundation of Korea (NRF) - Korean Government [Ministry of Science and ICT (MSIT)] [2020R1A2C2005836]
- National Research Foundation of Korea [2020R1A2C2005836] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
The study found that Lycopus lucidus Turcz (LLT) has a beneficial effect on dermatitis by inhibiting infiltration of inflammatory cells in skin tissue and suppressing the expression of pro-inflammatory cytokines. LLT also showed anti-inflammatory properties in both keratinocyte and macrophage cell models. Ultimately, LLT may be a promising candidate for the treatment of inflammatory dermatitis.
Atopic dermatitis (AD) is a chronic inflammatory allergic skin disease, characterized by pruritic and eczematous skin lesions. Lycopus lucidus Turcz (LLT) is a perennial herb that has been reported to have various biological properties, including effects on blood circulation, as well as anti-inflammatory, antioxidant, anti-vascular inflammation and wound-healing effects. However, whether LLT improves dermatitis and the underlying mechanisms has yet to be determined. The aim of the present study was to determine whether LLT can improve 2,4-dinitrochlorobenzene (DNCB)-induced dermatitis and to verify the inhibitory effect of LLT on the expression of chemokines and pro-inflammatory cytokines in the HaCaT immortalized keratinocyte cell line. In addition, the anti-inflammatory function of LLT in RAW264.7 mouse macrophages was investigated. In the DNCB-induced AD mouse model, LLT inhibited infiltration by mast cells, eosinophils and CD8(+) cells in the dorsal skin tissue of AD mice, and suppressed the expression of IgE and IL-6 in serum. In addition, LLT inhibited the phosphorylation of ERK and JNK, as well as NF-kappa B in skin tissue. In the HaCaT cell model induced by TNF-alpha/IFN-gamma, LLT inhibited the expression of thymus and activation-regulated chemokine, granulocyte-macrophage colony-stimulating factor, monocyte chemoattractant protein-1, TNF-alpha and IL-1 beta, whilst inhibiting the phosphorylation of NF-kappa B. In addition, in the lipopolysaccharide-induced RAW 264.7 cell inflammation model, LLT inhibited the expression of TNF-alpha and IFN-gamma, the nuclear translocation of NF-kappa B and the phosphorylation of ERK and JNK. These results suggested that LLT may be a promising candidate for the treatment of inflammatory dermatitis.
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