Hesperidin Attenuates Ultraviolet B-Induced Apoptosis by Mitigating Oxidative Stress in Human Keratinocytes.
10.4062/biomolther.2015.139
- Author:
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
Author Information
1. School of Medicine, Jeju National University, Jeju 63243, Republic of Korea. jinwonh@jejunu.ac.kr
- Publication Type:Original Article
- Keywords:
Apoptosis;
Antioxidant;
Hesperidin;
Reactive oxygen species;
Ultraviolet B
- MeSH:
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
- From:Biomolecules & Therapeutics
2016;24(3):312-319
- CountryRepublic 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.
