Title: The Flavonoid Luteolin Increases the Resistance of Normal, but Not Malignant Keratinocytes, Against UVB-Induced Apoptosis
Authors: Verschooten, Lien ×
Smaers, Katrien
Van Kelst, Sofie
Proby, Charlotte
Maes, Daniel
Declercq, Lieve
Agostinis, Patrizia
Garmyn, Maria #
Issue Date: Sep-2010
Publisher: Elsevier Science Pub. Co.
Series Title: Journal of Investigative Dermatology vol:130 issue:9 pages:2277-2285
Abstract: Adequate protection of skin against the carcinogenic effects of UVB irradiation is essential. Flavonoids may have a conspicuous role in cancer prevention because of their antioxidant, anti-inflammatory, and growth-inhibitory effects. Therefore, we tested the effects of the flavone luteolin (LUT) on selected parameters of the sunburn response in normal human keratinocytes, exposed to physiological doses of UVB. LUT attenuated UVB-induced cell death through delay and inhibition of intrinsic apoptotic signaling. Moreover, LUT not only predominantly affected the mitochondrial apoptosis pathway through its antioxidant capacity, but also changed the balance of Bcl2 (B-cell leukemia/lymphoma 2)-family members. Furthermore, LUT had inhibitory effects on the UVB-induced release of the inflammatory mediators, IL-1alpha and prostaglandin-E(2). Using different cell lines derived from squamous cell carcinomas, we showed that LUT did not increase the resistance of malignant keratinocytes to UVB. Our data suggest that LUT inhibits different aspects of the sunburn response, which results ultimately in an increased survival of normal keratinocytes, whereas the sensitivity of malignant cells to UVB remain unchanged. Hence, LUT might have value in new photoprotective applications or improve existing ones.Journal of Investigative Dermatology advance online publication, 13 May 2010; doi:10.1038/jid.2010.124.
ISSN: 0022-202X
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Laboratory of Dermatology
Laboratory of Cell Death Research & Therapy
× corresponding author
# (joint) last author

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