Ultraviolet B (UVB) irradiation may cause
inflammation- and oxidative-stress-dependent
skin cancer and
premature aging.
Naringenin (1) has been reported to have anti-inflammatory and
antioxidant properties, but its effects and mechanisms on UVB irradiation-induced
inflammation and oxidative stress are still not known. Thus, the present study aimed to investigate the potential of
naringenin to mitigate UVB irradiation-induced
inflammation and oxidative damage in the skin of hairless mice. Skin
edema,
myeloperoxidase (neutrophil marker) and
matrix metalloproteinase-9 (MMP-9) activity, and
cytokine production were measured after UVB irradiation. Oxidative stress was evaluated by
2,2'-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) radical (
ABTS) scavenging ability, ferric reducing
antioxidant power (FRAP),
reduced glutathione levels,
catalase activity, lipid peroxidation products,
superoxide anion production, and gp91phox (
NADPH oxidase subunit)
mRNA expression by quantitative PCR. The intraperitoneal treatment with
naringenin reduced skin
inflammation by inhibiting skin
edema, neutrophil recruitment, MMP-9 activity, and pro-inflammatory (TNF-α, IFN-γ, IL-1β, IL-4, IL-5, IL-6, IL-12, IL-13, IL-17, IL-22, and IL-23) and anti-inflammatory (TGF-β and IL-10)
cytokines.
Naringenin also inhibited oxidative stress by reducing
superoxide anion production and the
mRNA expression of gp91phox. Therefore,
naringenin inhibits UVB irradiation-induced skin damage and may be a promising therapeutic approach to control
skin disease.