Molecules (Aug 2007)

(-)-Epicatechin-3-gallate, a Green Tea Polyphenol Is a Potent Agent Against UVB-induced Damage in HaCaT Keratinocytes

  • Chi-Feng Hung,
  • Ying-Ting Chen,
  • Bing-Huei Chen,
  • Shao-Kuan Chen,
  • Han-Sun Chiang,
  • Jia-You Fang,
  • Wen-Bin Wu,
  • Chieh-Chen Huang

DOI
https://doi.org/10.3390/12081845
Journal volume & issue
Vol. 12, no. 8
pp. 1845 – 1858

Abstract

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(-)-Epicatechin-3-gallate (ECG) is a polyphenolic compound similar to (-)-epigallocatechin-3-gallate (EGCG) which is abundant in green tea. Numerous workers have proposed that EGCG protects epidermal cells against UVB-induced damage. However, little has been known about whether ECG protects keratinocytes against UVB-induced damage. We decided to investigate the protective effects and underlying mechanisms of ECG on UVB-induced damage. Cell viability was determined by the MTT assay. Activation of ERK1/2, p38 and JNK was analyzed by Western blotting. Intracellular H2O2 production and DNA content was analyzed by flow cytometry. Lipid peroxidation was assayed by colorimetry. In our study, we found that ECG dose-dependently attenuated UVB-induced keratinocyte death. Moreover, ECG markedly inhibited UVB-induced cell membrane lipid peroxidation and H2O2 generation in keratinocytes, suggesting that ECG can act as a free radical scavenger when keratinocytes were photodamaged. In parallel, H2O2-induced the activation of ERK1/2, p38 and JNK in keratinocytes could be inhibited by ECG. UVB-induced pre-G1 arrest leading to apoptotic changes of keratinocytes were blocked by ECG. Taken together, we provide here evidence that ECG protects keratinocytes from UVB-induced photodamage and H2O2-induced oxidative stress, possibly through inhibition of the activation of ERK1/2, p38 and JNK and/or scavenging of free radicals.

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