Grape seed proanthocyanidin extract protects human lens epithelial cells from oxidative stress via reducing NF-кB and MAPK protein expression

Zhiyan Jia,Z. Song,Yuhui Zhao,Xiu-dong Wang,Ping Liu

Published 2011 in Molecular Vision

ABSTRACT

Purpose Oxidative damage induced by H2O2 treatment can irreversibly damage the lens epithelium, resulting in cell death and cataract. Grape seed extract (GSE) is a widely consumed dietary supplement that has the capability to scavenge oxidants and free radicals. GSE contain 70%–95% standardized proanthocyanidins. The study described herein investigated the protective effect of Grape seed proanthocyanidin extract (GSPE) on H2O2-induced oxidative stress in human lens epithelial B-3 (HLEB-3) cells and the possible molecular mechanism involved. Methods HLE-B3 cells exposed to different doses of H2O2 were cultured with various concentrations of GSPE and subsequently monitored for cell viability by the 4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide (MTT) assay. The apoptosis rate and ROS generation were detected by flow cytometric analysis. Expression of NF-кB/P65 and mitogen activated protein kinase (MAPK) proteins were measured by western blot. Results GSPE clearly reduced H2O2 induced cell apoptosis and reactive oxygen species (ROS) generation and protected HLEB-3 cells from H2O2 induced oxidative damage. GSPE depressed H2O2-induced activation and translocation of NF-кB/p65. GSPE also depressed H2O2-induced phosphorylation of the p38 and c-Jun N-terminal kinase (JNK) proteins of the MAPK family at various time points studied. Conclusions GSPE could be useful in attenuation of H2O2-induced oxidative stress and the activation of NF-кB and MAPK signaling in HLE-B3 cells, which suggests that GSPE has a potential protective effect against cataractogenesis.

PUBLICATION RECORD

  • Publication year

    2011

  • Venue

    Molecular Vision

  • Publication date

    2011-01-20

  • Fields of study

    Biology, Medicine, Environmental Science

  • Identifiers
  • External record

    Open on Semantic Scholar

  • Source metadata

    Semantic Scholar, PubMed

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