(+)-Catechin prevents ultraviolet B-induced human keratinocyte death via inhibition of JNK phosphorylation

Abstract

High levels of (+)-catechin are found in the skin and seed of many fruits such as apples and grapes. Dietary supplementation with (+)-catechin has been demonstrated to protect epidermal cells against damage induced by ultraviolet B (UVB) radiation. However, the underlying mechanisms are not well understood yet. To determine whether (+)-catechin protects keratinocytes from UVB-induced damage, the viability of UVB- and H 2O 2-treated cells was determined by cell viability assay. Intracellular H 2O 2 level was measured by flow cytometry. UVB- or H 2O 2-induced signaling pathways were detected by Western blotting. The results indicated that (+)-catechin inhibited UVB- and H 2O 2-induced keratinocyte death. In parallel, intracellular H 2O 2 generation in keratinocytes irradiated by UVB was inhibited by (+)-catechin in a concentration-dependent manner. (+)-Catechin also inhibited UVB- and H 2O 2-induced JNK activation in keratinocytes. However, it had little inhibitory effect on UVB- and H 2O 2-induced ERK and p38 activation even at a higher concentration, suggesting indirectly that JNK activation is required for the induction of apoptosis in keratinocytes exposed to UVB. Finally, we compared the cytotoxicity of (+)-catechin and (−)-epigallocatechin-3-gallate (EGCG) on keratinocytes. Cell viability assay showed that (+)-catechin was relatively nontoxic at higher doses. Taken together, our results demonstrate that (+)-catechin inhibits UVB- and oxidative stress-induced H 2O 2 production and JNK activation and enhances human keratinocyte survival. However, although it seems that (+)-catechin and EGCG are equally effective in preventing keratinocyte death, (+)-catechin is relatively nontoxic and thus is suitable for developing as an anti-ageing agent for skin care.