<em>Lycopus lucidus</em> Turcz ameliorates DNCB‑induced atopic dermatitis in BALB/c mice

Min,Ga-Yul; Kim,Eun-Young; Hong,Sooyeon; Kim,Jae-Hyun; Kim,Minsun; Kim,Eom Ji; Park,Jae Ho; Sohn,Youngjoo; Jung,Hyuk-Sang

doi:10.3892/mmr.2021.12467

Lycopus lucidus Turcz ameliorates DNCB‑induced atopic dermatitis in BALB/c mice

Authors:
- Ga-Yul Min
- Eun-Young Kim
- Sooyeon Hong
- Jae-Hyun Kim
- Minsun Kim
- Eom Ji Kim
- Jae Ho Park
- Youngjoo Sohn
- Hyuk-Sang Jung
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Affiliations: Department of Anatomy, College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea, Department of Pharmaceutical Science, Jungwon University, Goesan, Chungbuk 28024, Republic of Korea
Published online on: September 27, 2021 https://doi.org/10.3892/mmr.2021.12467
Article Number: 827
Copyright: © Min et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

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‑κB in skin tissue. In the HaCaT cell model induced by TNF‑α/IFN‑γ, LLT inhibited the expression of thymus and activation‑regulated chemokine, granulocyte‑macrophage colony‑stimulating factor, monocyte chemoattractant protein‑1, TNF‑α and IL‑1β, whilst inhibiting the phosphorylation of NF‑κB. In addition, in the lipopolysaccharide‑induced RAW 264.7 cell inflammation model, LLT inhibited the expression of TNF‑α and IFN‑γ, the nuclear translocation of NF‑κB 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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