Tags

Type your tag names separated by a space and hit enter

Epigallocatechin gallate protects against oxidative stress-induced mitochondria-dependent apoptosis in human lens epithelial cells.

Abstract

PURPOSE

Oxidative stress has long been recognized as an important mediator of apoptosis in lens epithelial cells and also plays an important role in the pathogenesis of cataracts. (-)-Epigallocatechin gallate (EGCG), the most abundant component in green tea, has potent antioxidant activity. The goals of this study were to determine the protective effect of EGCG against H(2)O(2)-induced apoptotic death and the possible mechanisms involved in human lens epithelial (HLE) cells.

METHODS

HLEB-3, a human lens epithelial cell line, was exposed to various concentrations of H(2)O(2) and EGCG and subsequently monitored for cell death by the MTT assay and flow cytometric analysis using Annexin V and PI. The effect of EGCG in protecting HLE cells from cell death was determined by various assays after the cells were exposed to H(2)O(2). The ability of EGCG to block the accumulation of intracellular reactive oxygen species and the loss of mitochondrial membrane potential (Deltapsim) induced by H(2)O(2) was examined with dichlorofluorescein (DCF) fluorescence and 5,5',6,6'-tetrachloro-1,1',3,3'-tetrathylbenzimidazol carbocyanine iodide (JC-1). The expression of cytochrome c, caspase-9, caspase-3, and Bcl-2 family proteins was measured by western blotting. The changed expression of the mitogen activated protein kinase (MAPK) and Akt pathways was also detected by western blot.

RESULTS

In the present study, EGCG protected against cell death caused by H(2)O(2) in HLEB-3 cells. EGCG reduced the H(2)O(2)-induced generation of reactive oxygen species (ROS), the loss of mitochondrial membrane potential (Deltapsim), and the release of cytochrome c from the mitochondria into the cytosol. EGCG inhibited the H(2)O(2)-stimulated increase of caspase-9 and caspase-3 expression and the decrease of the Bcl-2/Bax ratio. Moreover, EGCG attenuated the reduced activation and expression of ERK, p38 MAPK, and Akt induced by H(2)O(2).

CONCLUSIONS

These findings suggest that EGCG protects HLE cells from the mitochondria-mediated apoptosis induced by H(2)O(2) through the modulation of caspases, the Bcl-2 family, and the MAPK and Akt pathways.

Links

  • PMC Free PDF
  • PMC Free Full Text
  • patent databases
  • Authors+Show Affiliations

    ,

    Eye Center, Affiliated Second Hospital, College of Medicine, Zhejiang University, Hangzhou, China. xlren@zju.edu.cn

    , , , ,

    Source

    Molecular vision 14: 2008 Jan 31 pg 217-23

    MeSH

    Apoptosis
    Caspase Inhibitors
    Catechin
    Cell Line
    Cytochromes c
    Cytosol
    Enzyme Activation
    Epithelial Cells
    Humans
    Hydrogen Peroxide
    Lens, Crystalline
    Membrane Potential, Mitochondrial
    Mitochondria
    Mitogen-Activated Protein Kinases
    Oxidative Stress
    Proto-Oncogene Proteins c-akt
    Proto-Oncogene Proteins c-bcl-2
    Reactive Oxygen Species

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    18334937

    Citation

    Yao, Ke, et al. "Epigallocatechin Gallate Protects Against Oxidative Stress-induced Mitochondria-dependent Apoptosis in Human Lens Epithelial Cells." Molecular Vision, vol. 14, 2008, pp. 217-23.
    Yao K, Ye P, Zhang L, et al. Epigallocatechin gallate protects against oxidative stress-induced mitochondria-dependent apoptosis in human lens epithelial cells. Mol Vis. 2008;14:217-23.
    Yao, K., Ye, P., Zhang, L., Tan, J., Tang, X., & Zhang, Y. (2008). Epigallocatechin gallate protects against oxidative stress-induced mitochondria-dependent apoptosis in human lens epithelial cells. Molecular Vision, 14, pp. 217-23.
    Yao K, et al. Epigallocatechin Gallate Protects Against Oxidative Stress-induced Mitochondria-dependent Apoptosis in Human Lens Epithelial Cells. Mol Vis. 2008 Jan 31;14:217-23. PubMed PMID: 18334937.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Epigallocatechin gallate protects against oxidative stress-induced mitochondria-dependent apoptosis in human lens epithelial cells. AU - Yao,Ke, AU - Ye,Panpan, AU - Zhang,Li, AU - Tan,Jian, AU - Tang,Xiajing, AU - Zhang,Yidong, Y1 - 2008/01/31/ PY - 2007/09/23/received PY - 2008/01/21/accepted PY - 2008/3/13/pubmed PY - 2008/5/7/medline PY - 2008/3/13/entrez SP - 217 EP - 23 JF - Molecular vision JO - Mol. Vis. VL - 14 N2 - PURPOSE: Oxidative stress has long been recognized as an important mediator of apoptosis in lens epithelial cells and also plays an important role in the pathogenesis of cataracts. (-)-Epigallocatechin gallate (EGCG), the most abundant component in green tea, has potent antioxidant activity. The goals of this study were to determine the protective effect of EGCG against H(2)O(2)-induced apoptotic death and the possible mechanisms involved in human lens epithelial (HLE) cells. METHODS: HLEB-3, a human lens epithelial cell line, was exposed to various concentrations of H(2)O(2) and EGCG and subsequently monitored for cell death by the MTT assay and flow cytometric analysis using Annexin V and PI. The effect of EGCG in protecting HLE cells from cell death was determined by various assays after the cells were exposed to H(2)O(2). The ability of EGCG to block the accumulation of intracellular reactive oxygen species and the loss of mitochondrial membrane potential (Deltapsim) induced by H(2)O(2) was examined with dichlorofluorescein (DCF) fluorescence and 5,5',6,6'-tetrachloro-1,1',3,3'-tetrathylbenzimidazol carbocyanine iodide (JC-1). The expression of cytochrome c, caspase-9, caspase-3, and Bcl-2 family proteins was measured by western blotting. The changed expression of the mitogen activated protein kinase (MAPK) and Akt pathways was also detected by western blot. RESULTS: In the present study, EGCG protected against cell death caused by H(2)O(2) in HLEB-3 cells. EGCG reduced the H(2)O(2)-induced generation of reactive oxygen species (ROS), the loss of mitochondrial membrane potential (Deltapsim), and the release of cytochrome c from the mitochondria into the cytosol. EGCG inhibited the H(2)O(2)-stimulated increase of caspase-9 and caspase-3 expression and the decrease of the Bcl-2/Bax ratio. Moreover, EGCG attenuated the reduced activation and expression of ERK, p38 MAPK, and Akt induced by H(2)O(2). CONCLUSIONS: These findings suggest that EGCG protects HLE cells from the mitochondria-mediated apoptosis induced by H(2)O(2) through the modulation of caspases, the Bcl-2 family, and the MAPK and Akt pathways. SN - 1090-0535 UR - https://www.unboundmedicine.com/medline/citation/18334937/Epigallocatechin_gallate_protects_against_oxidative_stress_induced_mitochondria_dependent_apoptosis_in_human_lens_epithelial_cells_ L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/18334937/ DB - PRIME DP - Unbound Medicine ER -