Wu Wen-Bin, Chiang Han-Sun, Fang Jia-You, Chen Shao-Kuan, Huang Chieh-Chen, Hung Chi-Feng
School of Medicine, Fu-Jen Catholic University, No. 510, Jhongjheng Rd., Sinjhuang City, Taipei County 24205, Taiwan ROC.
Life Sci. 2006 Jul 17;79(8):801-7. doi: 10.1016/j.lfs.2006.02.028. Epub 2006 Mar 29.
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 H2O2-treated cells was determined by cell viability assay. Intracellular H2O2 level was measured by flow cytometry. UVB- or H2O2-induced signaling pathways were detected by Western blotting. The results indicated that (+)-catechin inhibited UVB- and H2O2-induced keratinocyte death. In parallel, intracellular H2O2 generation in keratinocytes irradiated by UVB was inhibited by (+)-catechin in a concentration-dependent manner. (+)-Catechin also inhibited UVB- and H2O2-induced JNK activation in keratinocytes. However, it had little inhibitory effect on UVB- and H2O2-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 H2O2 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.
在许多水果（如苹果和葡萄）的果皮和种子中发现了高含量的（+）-儿茶素。膳食补充（+）-儿茶素已被证明可保护表皮细胞免受紫外线B（UVB）辐射诱导的损伤。然而，其潜在机制尚未完全清楚。为了确定（+）-儿茶素是否能保护角质形成细胞免受UVB诱导的损伤，通过细胞活力测定法测定了UVB和H2O2处理细胞的活力。通过流式细胞术测量细胞内H2O2水平。通过蛋白质印迹法检测UVB或H2O2诱导的信号通路。结果表明，（+）-儿茶素抑制UVB和H2O2诱导的角质形成细胞死亡。同时，（+）-儿茶素以浓度依赖的方式抑制UVB照射的角质形成细胞内H2O2的产生。（+）-儿茶素还抑制UVB和H2O2诱导的角质形成细胞中JNK的激活。然而，即使在较高浓度下，它对UVB和H2O2诱导的ERK和p38激活也几乎没有抑制作用，这间接表明JNK激活是UVB照射的角质形成细胞诱导凋亡所必需的。最后，我们比较了（+）-儿茶素和（-）-表没食子儿茶素-3-没食子酸酯（EGCG）对角质形成细胞的细胞毒性。细胞活力测定表明，（+）-儿茶素在较高剂量下相对无毒。综上所述，我们的结果表明，（+）-儿茶素抑制UVB和氧化应激诱导的H2O2产生和JNK激活，并提高人角质形成细胞的存活率。然而，尽管（+）-儿茶素和EGCG在预防角质形成细胞死亡方面似乎同样有效，但（+）-儿茶素相对无毒，因此适合开发为皮肤护理的抗衰老剂。
