ArticleAntioxidants (Basel, Switzerland)2022
The Inflammatory Response in Human Keratinocytes Exposed to Cinnamaldehyde Is Regulated by Nrf2.
Article in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Essential Oils as Antioxidants: Mechanistic Insights from Radical Scavenging to Redox Signaling.Antioxidants (Basel, Switzerland) · 2025Review
- Cinnamic Acid Derivatives as Potential Multifunctional Agents in Cosmetic Formulations Used for Supporting the Treatment of Selected Dermatoses.Molecules (Basel, Switzerland) · 2024Review
- Photobiomodulation Controls Keratinocytes Inflammatory Response through Nrf2 and Reduces Langerhans Cells Activation.Antioxidants (Basel, Switzerland) · 2023Article
- Cinnamon: an aromatic condiment applicable to chronic kidney disease.Kidney research and clinical practice · 2023Article
- Ethylhexadecyldimethylammonium bromide, a quaternary ammonium compound, controls inflammatory response through NRF2 pathway in a human immortalized keratinocyte cell line.Frontiers in toxicology · 2023Article
- The role of NRF2 transcription factor in inflammatory skin diseases.BioFactors (Oxford, England)Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keratinocytes (KC) play a crucial role in epidermal barrier function, notably through their metabolic activity and the detection of danger signals. Chemical sensitizers are known to activate the transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2), leading to cellular detoxification and suppressed proinflammatory cytokines such as IL-1β, a key cytokine in skin allergy. We investigated the role of Nrf2 in the control of the proinflammatory response in human KC following treatment with Cinnamaldehyde (CinA), a well-known skin sensitizer. We used the well-described human KC cell line KERTr exposed to CinA. Our results showed that 250 μM of CinA did not induce any Nrf2 accumulation but increased the expression of proinflammatory cytokines. In contrast, 100 μM of CinA induced a rapid accumulation of Nrf2, inhibited
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Registered trials
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