Journal of ethnopharmacology · 2026
Ethnopharmacological investigation of Elaeocarpus sylvestris leaf extract in mitigating atopic dermatitis-like lesions via inflammatory signaling modulation.
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Kim So-Yeon, Do Young-Ju, Lee Su-Jung, Cho Ye Eun, Cho So-Young, Lee Ye-Won, Lee Seon-Woo, Lee Na-Hyun, Bae Ji-Yeong, Lee Sanghyun, Lee Sang Ho, Park Se Jin
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Historically, Elaeocarpus sylvestris has served as a traditional medicinal agent for inflammatory disorders across East Asia. Recent studies have reported its antioxidant and anti-inflammatory activities, supporting its potential as a natural therapeutic resource for inflammatory skin diseases such as atopic dermatitis (AD). However, its pharmacological relevance to AD and the cellular signaling cascades remain insufficiently elucidated.
AIM OF THE STUDY: This study aimed to pharmacologically validate the traditional use of E. sylvestris by investigating the anti-inflammatory and anti-atopic effects of its leaf ethanol extract (ESLE) and elucidating the associated molecular mechanisms.
MATERIALS AND METHODS: Inflammatory profiles of LPS-primed HaCaT cells were analyzed to evaluate the bioactivity of ESLE. We employed western blotting to dissect the intracellular signaling networks, focusing on the IRAK4-mediated MAPK, NF-κB, and JAK/STAT pathways. The study also extended to a DNCB-induced murine model of AD, facilitating a comprehensive assessment of efficacy of ESLE through histopathological examination and transepidermal water loss measurements.
RESULTS: Geraniin was confirmed as a representative biomarker to verify ESLE's identity. ESLE significantly inhibited NO and PGE2 production by downregulating iNOS and COX-2, while reducing pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) in keratinocytes. These effects were mediated by the suppression of IRAK4-dependent MAPK, NF-κB, and JAK/STAT signaling. Furthermore, ESLE improved skin barrier function and attenuated AD hallmarks, including mast cell infiltration, serum IgE elevation, and lymphoid organ hypertrophy.
CONCLUSIONS: ESLE attenuates inflammatory responses and improves AD-like symptoms, potentially through modulation of inflammation-related signaling pathways. These findings support the pharmacological relevance of E. sylvestris and its traditional use in inflammatory skin conditions.
AIM OF THE STUDY: This study aimed to pharmacologically validate the traditional use of E. sylvestris by investigating the anti-inflammatory and anti-atopic effects of its leaf ethanol extract (ESLE) and elucidating the associated molecular mechanisms.
MATERIALS AND METHODS: Inflammatory profiles of LPS-primed HaCaT cells were analyzed to evaluate the bioactivity of ESLE. We employed western blotting to dissect the intracellular signaling networks, focusing on the IRAK4-mediated MAPK, NF-κB, and JAK/STAT pathways. The study also extended to a DNCB-induced murine model of AD, facilitating a comprehensive assessment of efficacy of ESLE through histopathological examination and transepidermal water loss measurements.
RESULTS: Geraniin was confirmed as a representative biomarker to verify ESLE's identity. ESLE significantly inhibited NO and PGE2 production by downregulating iNOS and COX-2, while reducing pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) in keratinocytes. These effects were mediated by the suppression of IRAK4-dependent MAPK, NF-κB, and JAK/STAT signaling. Furthermore, ESLE improved skin barrier function and attenuated AD hallmarks, including mast cell infiltration, serum IgE elevation, and lymphoid organ hypertrophy.
CONCLUSIONS: ESLE attenuates inflammatory responses and improves AD-like symptoms, potentially through modulation of inflammation-related signaling pathways. These findings support the pharmacological relevance of E. sylvestris and its traditional use in inflammatory skin conditions.