Biomol Ther.  2016 May;24(3):312-319. 10.4062/biomolther.2015.139.

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

• Hewage SR
• Piao MJ
• Kang KA
• Ryu YS
• Han X
• Oh MC
• Jung U
• Kim IG
• Hyun JW

• KMID: 2164224
• DOI: http://doi.org/10.4062/biomolther.2015.139

Abstract

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 (C28H34O15) 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.

Keyword

Apoptosis; Antioxidant; Hesperidin; Reactive oxygen species; Ultraviolet B

MeSH Terms

Absorption
Apoptosis*
bcl-2-Associated X Protein
Caspase 3
Caspase 9
Cytochromes c
Cytosol
Hesperidin*
Humans*
Keratinocytes*
Lymphoma, B-Cell
Mitochondrial Membranes
Oxidative Stress*
Reactive Oxygen Species
Skin
Caspase 3
Caspase 9
Cytochromes c
Hesperidin
Reactive Oxygen Species
bcl-2-Associated X Protein