Hesperidin Attenuates Ultraviolet B-Induced Apoptosis by Mitigating Oxidative Stress in Human Keratinocytes

Human skin cells undergo pathophysiological processes via generation of reactive oxygen species (ROS) upon excessive exposure to ultraviolet B (UVB) radiation. This study investigated the ability of hesperidin (C(28)H(34)O(15)) to prevent apoptosis due to oxidative stress generated through UVB-induc...

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Detalles Bibliográficos
Autores principales: Hewage, Susara Ruwan Kumara Madduma, Piao, Mei Jing, Kang, Kyoung Ah, Ryu, Yea Seong, Han, Xia, Oh, Min Chang, Jung, Uhee, Kim, In Gyu, Hyun, Jin Won
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Applied Pharmacology 2016
Materias:
Original Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4859795/
https://www.ncbi.nlm.nih.gov/pubmed/26797112
http://dx.doi.org/10.4062/biomolther.2015.139
Descripción
Sumario:Human skin cells undergo pathophysiological processes via generation of reactive oxygen species (ROS) upon excessive exposure to ultraviolet B (UVB) radiation. This study investigated the ability of hesperidin (C(28)H(34)O(15)) to prevent apoptosis due to oxidative stress generated through UVB-induced ROS. Hesperidin significantly scavenged ROS generated by UVB radiation, attenuated the oxidation of cellular macromolecules, established mitochondrial membrane polarization, and prevented the release of cytochrome c into the cytosol. Hesperidin downregulated expression of caspase-9, caspase-3, and Bcl-2-associated X protein, and upregulated expression of B-cell lymphoma 2. Hesperidin absorbed wavelengths of light within the UVB range. In summary, hesperidin shielded human keratinocytes from UVB radiation-induced damage and apoptosis via its antioxidant and UVB absorption properties.

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