Original ContributionGrape seed proanthocyanidins inhibit UV-radiation-induced oxidative stress and activation of MAPK and NF-κB signaling in human epidermal keratinocytes
Section snippets
Chemicals and antibodies
GSPs were kindly provided by the Kikkoman Corp. (Japan), as a generous gift for our research work. Dihydrorhodamine 123 (DHR) was purchased from Molecular Probes (Eugene, OR, USA). OxyBlot Protein Oxidation Detection Kit was purchased from the Intergen Co. (Purchase, NY, USA). The phosphorylated ERK1/2 (Thr202/Tyr204), JNK (Thr183/Tyr185), and p38 (Thr180/Tyr182) and nonphosphorylated ERK1/2, JNK, and p38 antibodies and the anti-β-actin antibody were purchased from Cell Signaling Technology,
GSPs inhibit UVB-induced intracellular release of H2O2 in NHEK
Based on our prior studies with UVB and NHEK [14], NHEK were exposed to a UVB dose of 30 mJ/cm2, which resulted in more than 12-fold induction of intracellular release of H2O2 (Fig. 1A), which was determined as a marker of UVB-induced oxidative stress. Pretreatment of NHEK cells with GSPs (10–50 μg/ml) before UVB (30 mJ/cm2) exposure resulted in a dose-dependent inhibition of UVB-induced intracellular release of H2O2 (30–89%; *p < 0.01, ¶p < 0.001) when measured in terms of relative
Discussion
The UVB (290–320 nm) component of solar ultraviolet radiation acts as a tumor initiator, a tumor promoter, and a complete carcinogen [20]. It has been recognized that UVB-induced oxidative stress in an in vitro or in vivo system contributes to several adverse biological effects on the skin [1], [2], [21]. There is considerable evidence that the tumor-promoting effects of UVB radiation are mediated through UVB-induced oxidative stress-mediated activation of signal transduction pathways that
Acknowledgments
This work was supported by funds from USPHS Grant CA104428, the Merit Review Award from the Veterans Administration, and the UAB Skin Diseases Research Center (AR050948-01).
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