To assess the effects of hydroxysafflor yellow A (HSYA) on ultraviolet A (UVA)-induced damage in HaCaT keratinocytes. HaCaT keratinocytes were UVA-irradiated, and the effects of HSYA on cell viability, reactive oxygen species (ROS) generation, lipid peroxidation, and messenger (m)RNA expression were measured. mRNA expressions of matrix metalloproteinase (MMP)-1, MMP-2, MMP-9, and cyclooxygenase (COX)-2 were determined by a real-time polymerase chain reaction (RT-PCR). UVA exposure led to a decrease in cell viability and an increase in ROS generation in HaCaT keratinocytes. HSYA effectively increased the viability of HaCaT keratinocytes after UVA exposure and protected them from UVA-induced oxidative stress. Moreover, HSYA inhibited expressions of MMP-1, MMP-2, MMP-9, and COX-2 by HaCaT keratinocytes with UVA-induced photodamage. Our results suggest that HSYA can act as a free radical scavenger when keratinocytes are photodamaged. HSYA has the potential to be a skin-protective ingredient against UVA-induced photodamage.
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http://dx.doi.org/10.3390/ijms25147573 | DOI Listing |
Curr Mol Med
January 2025
Laboratory of Physicochemical and Genetic Problems in Dermatology, Center of Theoretical Problems in Physico-Chemical Pharmacology at Russian Academy of Sciences, Moscow Russia.
Background: The transcription factor AP1 plays a crucial role in the proliferation, apoptosis, and terminal differentiation of epidermal keratinocytes.
Objective: This study aimed to clarify whether the subunit of AP1, FOSL1 protein, can be used to assess the exacerbation of psoriasis by evaluating its changes in protein and mRNA levels in cultured epidermal keratinocytes and skin specimens of the patients prescribed with bathwater PUVA (Psoralen and UVA) therapy. This study aimed to investigate FOSL1, a subunit of the transcription factor AP-1, as a potential biomarker for psoriasis by examining its protein and mRNA expression in skin specimens from patients undergoing bathwater PUVA (Psoralen and UVA) therapy and cultured epidermal keratinocytes.
Bioinorg Chem Appl
January 2025
Institut Pasteur de Tunis, LR20IPT01 Biomolécules, Venins et Application Théranostiques (LBVAT), University of Tunis El Manar, Tunis 1002, Tunisia.
The efficacy of available treatments for melanoma is limited by side effects and the rapidly emerging resistance to treatment. In this context, the decavanadate compounds represent promising tools to design efficient therapeutic agents. In our study, we synthesized a dimagnesium disodium decavanadate icosahydrate compound (MgNaVO·20HO) and investigated its structure stability as well as its antimelanoma effects.
View Article and Find Full Text PDFFront Microbiol
January 2025
Doctoral Program of Biosciences, School of Engineering, Universidad de La Sabana, Chía, Cundinamarca, Colombia.
Marine-derived actinobacteria isolated from sponge and soft coral were screened for antibacterial activity against acne-related bacteria, specifically ATCC 14990, methicillin-resistant ATCC BAA44, and ATCC 6919. Cytotoxicity assays were performed on human dermal fibroblast (HDFa) and keratinocyte (HaCaT) cell lines to assess the safety profile of the extracts. Chemical characterization was conducted using high-performance liquid chromatography coupled with tandem mass spectrometry (HPLC-MS/MS).
View Article and Find Full Text PDFSci Rep
January 2025
Department of Veterinary Physiology, College of Veterinary Medicine, Gyeongsang National University, Gazwa, Jinju, 52828, Republic of Korea.
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by immune dysregulation and excessive cytokine production. This study aimed to explore the potential of Camellia sinensis L. water extract (CSE) as a treatment for AD by the impact of CSE on inflammatory responses in keratinocytes, particularly concerning the production of inflammatory cytokines and the modulation of signaling pathways relevant to AD pathogenesis.
View Article and Find Full Text PDFArch Dermatol Res
January 2025
Department of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
We have recently shown that fluoxetine (FX) suppressed polyinosinic-polycytidylic acid-induced inflammatory response and endothelin release in human epidermal keratinocytes, via the indirect inhibition of the phosphoinositide 3-kinase (PI3K)-pathway. Because PI3K-signaling is a positive regulator of the proliferation, in the current, highly focused follow-up study, we assessed the effects of FX (14 µM) on the proliferation and differentiation of human epidermal keratinocytes. We found that FX exerted anti-proliferative actions in 2D cultures (HaCaT and primary human epidermal keratinocytes [NHEKs]; 48- and 72-h; CyQUANT-assay) as well as in 3D reconstructed epidermal equivalents (48-h; Ki-67 immunohistochemistry).
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