Peucedanum japonicum Thunberg root extract inhibits atopic dermatitis-like skin symptoms
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Jang Hoon Kim [2] ; Kyung-Sook Han [2] ; Eun Seo Kang [1] ; Ji Hyeon Park [3] ; Byoung Ok Cho [3] ; Jae Ho Choi [4]
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[1] Jeonju University
Jeonju University
Corea del Sur
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[2] Department of Herbal Crop Research, National Institute of Horticultural & Herbal Science, RDA, Eumsung, Republic of Korea.
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[3] Institute of Health Science, Jeonju University, Jeonju-si, Jeollabuk-do, Republic of Korea.
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[4] Inflamm-Aging Translational Research Center, Ajou University Medical Center, Suwon, Republic of Korea; Department of Hematology-Oncology, Ajou University School of Medicine, Suwon, Republic of Korea.
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- Localización: Allergologia et immunopathologia: International journal for clinical and investigate allergology and clinical immunology, ISSN-e 1578-1267, ISSN 0301-0546, Vol. 53, Nº. 5, 2025, págs. 12-29
- Idioma: inglés
- Enlaces
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Resumen
Peucedanum japonicum Thunberg is a perennial herbaceous plant of the genus Peucedanum that belongs to the Apiaceae family and is effective in improving inflammation, gout, and dizziness. However, the skin pruritus improvement effect and mechanism of action of Peucedanum japonicum Thunberg root extract (PJRE) have not yet been reported. We investigated the effects of PJRE on the regulation of pruritus and inflammatory responses in compound 48/80 (C48/80)-treated mice, phorbol 12-myristate 13-acetate (PMA)/A23187-induced human skin mast cells, and LPS-stimulated mouse macrophages. PJRE administration significantly inhibited scratching behavior, skin inflammatory cells, and mast cell infiltration in mice increased by C48/80. PJRE treatment also reduced the PMA/A23187-activated secretion of histamine, inflammatory cytokines, and interleukins via NF-κB activation in HMC-1 cells. PJRE treatment reduced LPS-stimulated secretion of inflammatory cytokines and expression of iNOS and COX-2 through phosphorylation of NF-κB, Akt, ERK1/2, and p38 MAPK in Raw 264.7 cells. PJRE treatment increases HO-1 expression in a concentration-dependent manner via NRF2 nuclear translocation. These results suggest that PJRE has therapeutic potential for alleviating atopic dermatitis-like skin symptoms, which is likely mediated by NF-κB as a transcription factor and Akt, ERK1/2, and p38 MAPK as upstream signaling molecules.
