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Methyl gallate protects against oxidative stress‐induced apoptosis in PC12 cells
Author(s) -
Crispo James,
Piché Matthew,
Ansell Dominique,
Eibl Joseph,
Tai Isabella,
Ross Gregory,
Tai T.C.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.lb483
Subject(s) - apoptosis , oxidative stress , viability assay , mitochondrion , intracellular , epigallocatechin gallate , chemistry , gallic acid , microbiology and biotechnology , dna damage , polyphenol , glutathione , gallate , biochemistry , pharmacology , biology , antioxidant , dna , enzyme
Recent studies demonstrate that polyphenols reduce oxidative damage by increasing cell viability, decreasing intracellular ROS and altering GSH metabolism. In addition, polyphenols such as epigallocatechin gallate (EGCG) have been reported to inhibit apoptotic signaling and increase neural cell survival. In an effort to better understand the benefits associated with polyphenol consumption, the aim of this study was to investigate potential anti‐apoptotic effects of EGCG, methyl gallate (MG), gallic acid (GA) and N‐acetylcysteine (NAC) on H2O2‐induced apoptosis in PC12 cells and elucidate protective mechanisms. Pre‐treatment with MG and NAC significantly increase viability of H2O2‐stressed cells, while pre‐treatments with EGCG and GA exacerbates stress. Analyses of apoptosis and mitochondrial membrane potential reveals that MG pre‐treatment prevents mitochondria depolarization, however does not inhibit apoptosis. Further, analysis of DNA degradation and caspase cleavage shows that MG inhibits activation of caspase 9 and has a partial inhibitory effect on DNA degradation. These findings suggest that MG may have potential therapeutic properties against mitochondria‐mediated apoptosis. Research funded by the Northern Ontario School of Medicine and Natural Sciences and Engineering Research Council of Canada.