Inhibition of UVB-induced oxidative stress-mediated phosphorylation of mitogen-activated protein kinase signaling pathways in cultured human epidermal keratinocytes by green tea polyphenol (-)-epigallocatechin-3-gallate
Inhibition of UVB-induced oxidative stress-mediated phosphorylation of mitogen-activated protein kinase signaling pathways in cultured human epidermal keratinocytes by green tea polyphenol (-)-epigallocatechin-3-gallate
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DOI：
10.1006/taap.2001.9276
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发表时间：
2001-10-15
影响因子：
3.8
通讯作者：
Mukhtar, H
中科院分区：
文献类型：
--
作者：
Katiyar, SK;Afaq, F;Mukhtar, H
正常人表皮角质形成细胞（NHEK）暴露于UVB辐射诱导细胞内过氧化氢（氧化应激）的释放和有丝分裂原活化蛋白激酶细胞信号通路的磷酸化。在这里，我们证明，（-）-表没食子儿茶素-3-没食子酸酯（EGCG），从绿色茶的抗氧化剂，预处理NHEK抑制UVB诱导的过氧化氢（H2 O2）的生产和H2 O2介导的MAPK信号通路的磷酸化。我们发现，在UVB（30 mJ/cm（2））暴露之前，将EGCG（20 μ g/ml培养基）处理NHEK，抑制UVB诱导的H2 O2产生（66-80%），同时抑制UVB诱导的ERK 1/2（57-80%）、JNK（53-83%）和p38（50-77%）蛋白的磷酸化。证明UVB是否诱导磷酸化。通过UVB诱导的H_2O_2（氧化应激）产生的MAPK的发生，用氧化剂H_2O_2处理NHEK。H2 O2对NHEK的处理导致ERK 1/2、JNK和p38的磷酸化。使用相同的体外系统，当这些细胞用EGCG或已知的抗氧化剂抗坏血酸（作为阳性对照）预处理时，发现H2 O2诱导的ERK 1/2、JNK和p38磷酸化被显著抑制。这些研究结果表明，表没食子儿茶素没食子酸酯具有抑制UVB诱导的氧化应激介导的MAPK信号通路磷酸化的潜力，表明表没食子酸酯可用于减轻氧化应激介导的和MAPK引起的人类皮肤病。(C)北京：科学出版社.
Exposure of normal human epidermal keratinocytes (NHEK) to UVB radiation induces intracellular release of hydrogen peroxide (oxidative stress) and phosphorylation of mitogen-activated protein kinase cell signaling pathways. Here, we demonstrate that pretreatment of NHEK with (-)-epigallocatechin-3-gallate (EGCG), an antioxidant from green tea, inhibits UVB-induced hydrogen peroxide (H2O2) production and H2O2-mediated phosphorylation of MAPK signaling pathways. We found that treatment of EGCG (20 mug/ml of media) to NHEK before UVB (30 mJ/cm(2)) exposure inhibited UVB-induced H2O2 production (66-80%) concomitant with the inhibition of UVB-induced phosphorylation of ERK1/2 (57-80%), JNK (53-83%), and p38 (50-77%) proteins. To demonstrate whether UVB-induced phosphorylation. of MAPK occurs via UVB-induced H2O2 (oxidative stress) production, NHEK were treated with the oxidant H2O2. Treatment of H2O2 to NHEK resulted in phosphorylation of ERK1/2, JNK, and p38. Using the same in vitro system, when these cells were pretreated with EGCG or with the known antioxidant ascorbic acid (as positive control), H2O2-induced phosphorylation of ERK1/2, JNK, and p38 was found to be significantly inhibited. These findings demonstrate that EGCG has the potential to inhibit UVB-induced oxidative stress-mediated phosphorylation of MAPK signaling pathways, suggesting that EGCG could be useful in attenuation of oxidative stress-mediated and MAPK-caused skin disorders in humans. (C) 2001 Academic Press.