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

Author:

Kwon Yujin12ORCID,Kang Yoon Jin13ORCID,Kwon Jaeyoung24ORCID,Cho Su‐Yeon12ORCID,Kim Jiyoon5ORCID,Le Tam Thi1ORCID,Hwang Hoseong46ORCID,Deshar Barsha5ORCID,Kim Myungjun7ORCID,Kim Ju Yeong7ORCID,Jung Jae Hung8ORCID,Kim Hyung‐Sik9ORCID,Jung Sang Hoon12ORCID,Kwon Hak Cheol4ORCID,Kim Won Kyu110ORCID

Affiliation:

1. Natural Product Research Center Korea Institute of Science and Technology (KIST) Gangneung Korea

2. Division of Bio‐Medical Science & Technology University of Science and Technology (UST) Daejeon Korea

3. Department of Marine Life Sciences, College of Life Science Gangneung‐Wonju National University Gangneung Korea

4. Natural Product Informatics Research Center Korea Institute of Science and Technology (KIST) Gangneung Korea

5. Department of Pharmacology, Department of Biomedicine & Health Sciences, College of Medicine The Catholic University of Korea Seoul Korea

6. Department of Biology Gangneung‐Wonju National University Gangneung Korea

7. Department of Tropical Medicine, Institute of Tropical Medicine, and Arthropods of Medical Importance Resource Bank Yonsei University College of Medicine Seoul Korea

8. Department of Urology Yonsei University Wonju College of Medicine/Center of Evidence Based Medicine Institute of Convergence Science Wonju Korea

9. Department of Oral Biochemistry, Dental and Life Science Institute, School of Dentistry Pusan National University Yangsan Korea

10. Department of Convergence Medicine Yonsei University Wonju College of Medicine Wonju Korea

Abstract

AbstractBackgroundAtopic 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.MethodsWe 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.ResultsFVE 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.ConclusionForsythia 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.

Funder

Korea Institute of Science and Technology

National Research Foundation of Korea

Publisher

Wiley

Subject

Immunology,Immunology and Allergy

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