ArticlePharmaceutical biology2025
Cedrol prevents UVB-induced photoaging by restoring mitochondrial function, metabolic homeostasis, and skin barrier integrity in HaCaT cells.
Article in Pharmaceutical biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Multi-Target Photoprotection by Taxifolin Against UVB-Induced Keratinocyte Injury Through UVB Filtration, ROS Scavenging and Transcriptomic-Proteomic Reprogramming.Biomolecules · 2026Article
- Seed Oil ofInternational journal of molecular sciences · 2026Article
- Alpinia zerumbet-Derived Extracellular Vesicles Protect Against UVB-Induced Photoaging by Enhancing Mitochondrial Bioenergetics and Skin Barrier Function.BioFactors (Oxford, England)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextUltraviolet B (UVB) radiation is a key environmental contributor to skin photoaging, primarily by inducing oxidative stress, mitochondrial dysfunction, metabolic imbalance, and downregulation of tight junction (TJ) proteins. Cedrol, the major component of the essential oil from
objectiveIn this study, HaCaT keratinocytes were used to evaluate the post-treatment effects of cedrol on UVB-induced damage to skin cells. MATERIALS AND
methodsHaCaT cells were exposed to UVB irradiation followed by cedrol treatment. Cell viability, intracellular reactive oxygen species (ROS), mitochondrial membrane potential, ATP levels, mitochondrial biogenesis-related proteins (SIRT1, PGC-1α, Nrf2, TFAM), and TJ proteins (ZO-1, occludin, claudin-3) were assessed. Additionally,
resultsCedrol significantly improved cell viability post-UVB exposure, decreased intracellular reactive oxygen species (ROS), and restored mitochondrial membrane potential and ATP levels. It also upregulated mitochondrial biogenesis-related proteins (SIRT1, PGC-1α, Nrf2, and TFAM) and maintained TJ protein expression (ZO-1, occludin, and claudin-3), thereby preserving epithelial barrier integrity. Furthermore, DISCUSSION AND
conclusionCedrol alleviates UVB-induced cellular damage by modulating mitochondrial function and metabolic homeostasis, indicating its potential as a natural agent for promoting skin recovery after UV exposure.
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Registered trials
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.