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. 2024 May;79(5):1242-1257.
doi: 10.1111/all.15967. Epub 2023 Dec 1.

Forsythia velutina Nakai extract: A promising therapeutic option for atopic dermatitis through multiple cell type modulation

Yujin Kwon  1   2 , Yoon Jin Kang  1   3 , Jaeyoung Kwon  2   4 , Su-Yeon Cho  1   2 , Jiyoon Kim  5 , Tam Thi Le  1 , Hoseong Hwang  4   6 , Barsha Deshar  5 , Myungjun Kim  7 , Ju Yeong Kim  7 , Jae Hung Jung  8 , Hyung-Sik Kim  9 , Sang Hoon Jung  1   2 , Hak Cheol Kwon  4 , Won Kyu Kim  1   10
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Forsythia velutina Nakai extract: A promising therapeutic option for atopic dermatitis through multiple cell type modulation

Yujin Kwon et al. Allergy. 2024 May.

Abstract

Background: Atopic dermatitis (AD) is a complex condition characterized by impaired epithelial barriers and dysregulated immune cells. In this study, we demonstrated Forsythia velutina Nakai extract (FVE) simultaneously inhibits basophils, macrophages, keratinocytes, and T cells that are closely interrelated in AD development.

Methods: We analyzed the effect of FVE on nitric oxide and reactive oxygen species (ROS) production in macrophages, basophil degranulation, T cell activation, and tight junctions in damaged keratinocytes. Expression of cell-type-specific inflammatory mediators was analyzed, and the underlying signaling pathways for anti-inflammatory effects of FVE were investigated. The anti-inflammatory effects of FVE were validated using a DNCB-induced mouse model of AD. Anti-inflammatory activity of compounds isolated from FVE was validated in each immune cell type.

Results: FVE downregulated the expression of inflammatory mediators and ROS production in macrophages through TLR4 and NRF2 pathways modulation. It significantly reduced basophil degranulation and expression of type 2 (T2) and pro-inflammatory cytokines by perturbing FcεRI signaling. Forsythia velutina Nakai extract also robustly inhibited the expression of T2 cytokines in activated T cells. Furthermore, FVE upregulated the expression of tight junction molecules in damaged keratinocytes and downregulated leukocyte attractants, as well as IL-33, an inducer of T2 inflammation. In the AD mouse model, FVE showed superior improvement in inflammatory cell infiltration and skin structure integrity compared to dexamethasone. Dimatairesinol, a lignan dimer, was identified as the most potent anti-inflammatory FVE compound.

Conclusion: Forsythia velutina Nakai extract and its constituent compounds demonstrate promising efficacy as a therapeutic option for prolonged AD treatment by independently inhibiting various cell types associated with AD and disrupting the deleterious link between them.

Keywords: Forsythia velutina Nakai; atopic dermatitis; epithelial barrier; inflammation; natural product.

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References

REFERENCES

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