Biomolecules & Therapeutics  2016;24(3):312-319

doi:10.4062/biomolther.2015.139

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

Susara Ruwan Kumara Madduma HEWAGE 1 ; Mei Jing PIAO ; Kyoung Ah KANG ; Yea Seong RYU ; Xia HAN ; Min Chang OH ; Uhee JUNG ; In Gyu KIM ; Jin Won HYUN

Affiliations

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Keywords

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

Country

Republic of Korea

Language

English

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.