Evidence map›Paper›PMID 41285703›Full record

ArticleNutrition & diabetes2025

Umbelliferone preserves skin epidermal barrier integrity in diabetes-induced keratinocytes by regulating actin dynamics and suppressing ROS-mediated apoptosis.

Dong Yeon Kim, Young-Hee Kang, Min-Kyung Kang

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Article in Nutrition & diabetes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Dong Yeon KimDepartment of Food and Nutrition, Gyeongkuk National University, Andong-si, Gyeongsangbuk-do, Republic of Korea.
Young-Hee KangDepartment of Food Science and Nutrition, Hallym University, Chuncheon-si, Gangwon-do, Republic of Korea.
Min-Kyung KangDepartment of Food and Nutrition, Gyeongkuk National University, Andong-si, Gyeongsangbuk-do, Republic of Korea. mkkang@gknu.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe skin serves as a fundamental protective barrier against environmental insults, with the epidermis, particularly the stratum corneum and tight junctions (TJs) connecting keratinocytes, playing a crucial role. Chronic hyperglycemia can impair these TJs, leading to compromised epidermal barrier function and diabetic skin complications. This study aimed to investigate the effects of umbelliferone on epidermal barrier function under type 2 diabetic conditions.

methodsHaCaT keratinocytes were cultured under hyperglycemic conditions induced by 33 mM glucose with or without 1-20 μM umbelliferone to evaluate cellular protection and barrier-related protein regulation. Type 2 diabetic db/db mice were administered umbelliferone orally at 10 mg/kg per day for 10 weeks. The expression of epidermal barrier-related proteins in HaCaT cells and skin tissues was quantified by Western blot analysis.

resultsUmbelliferone enhanced multiple components essential for maintaining the skin barrier. It upregulated filaggrin, increased the expression of the TJ proteins ZO-1 and Occludin, and elevated AQP3 and HAS2 levels to support epidermal hydration, while reducing HYAL1 expression. Under impaired wound healing conditions induced by hyperglycemia, umbelliferone promoted cell migration via modulation of F-actin organization, Rho GTPase signaling, and integrin β1 expression. Additionally, it reduced ROS accumulation and alleviated high glucose-induced apoptosis.

conclusionsUmbelliferone preserves epidermal barrier integrity by strengthening cell-cell junctions, enhancing hydration, promoting cell migration, and providing protection against oxidative stress and apoptosis. These findings suggest the therapeutic potential of umbelliferone in managing and preventing diabetic skin complications.

Indexed as

ApoptosisDiabetes Mellitus, Type 2EpidermisKeratinocytesReactive Oxygen SpeciesUmbelliferonesAnimalsFilaggrin ProteinsHaCaT CellsHumansMaleMiceTight Junctions7-hydroxycoumarinFilaggrin ProteinsFLG protein, humanReactive Oxygen SpeciesUmbelliferones

Identifiers

PMID41285703
PMCPMC12644754

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.