Hesperidin Attenuates Ultraviolet B-Induced Apoptosis by Mitigating Oxidative Stress in Human Keratinocytes
Biomolecules & Therapeutics
; : 312-319, 2016.
Article
in English
| WPRIM (Western Pacific)
| ID: wpr-51941
Responsible library:
WPRO
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.
Full text:
Available
Health context:
SDG3 - Target 3.4 Reduce premature mortality due to noncommunicable diseases
Health problem:
Lymphomas and Multiple Myeloma
Database:
WPRIM (Western Pacific)
Main subject:
Skin
/
Keratinocytes
/
Lymphoma, B-Cell
/
Reactive Oxygen Species
/
Apoptosis
/
Oxidative Stress
/
Cytosol
/
Cytochromes c
/
Absorption
/
Mitochondrial Membranes
Limits:
Humans
Language:
English
Journal:
Biomolecules & Therapeutics
Year:
2016
Document type:
Article