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Epigallocatechin‐3‐gallate Suppressed Methylglyoxal‐Induced Apoptosis in SH‐SY5Y Cells
Author(s) -
Cheng AnChin,
Lee MingFen,
Huang TzuLi,
Liou YiSiou,
Pan MinHsiung
Publication year - 2018
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.2018.32.1_supplement.664.10
Subject(s) - glycation , apoptosis , methylglyoxal , sh sy5y , mapk/erk pathway , chemistry , epigallocatechin gallate , programmed cell death , intracellular , pharmacology , biochemistry , kinase , microbiology and biotechnology , polyphenol , antioxidant , biology , cell culture , enzyme , receptor , genetics , neuroblastoma
Glycation is an endogenous process that generates a class of compounds known as advanced glycation end products (AGEs). AGEs are found in age‐related intracellular protein deposits of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Green tea polyphenols have a role in the reversal of age‐related loss of neuronal plasticity and recovery after neuronal lesions. There are several polyphenolic catechins in green tea, where epigallocatechin‐3‐gallate (EGCG) is both the most abundant and most biologically active form. EGCG could exhibit protective effects against AGEs‐induced injury in neuronal cells through its antioxidative properties, suggesting a beneficial role for this tea catechin against neurodegenerative diseases. In the current study, efforts were made to investigate the effects of EGCG on MG‐induced apoptosis. SH‐SY5Y cell were treated with different concentrations of EGCG followed by treatment with MG. Our data exhibited that both the cleaved PARP and cleaved‐caspase‐3 were downregulated by EGCG, and the MG‐induced reduction of Bcl‐2 expression were reversed by EGCG treatment. Moreover, EGCG could protect cells from death via reverse MG‐induced promoting of ERK/JNK pathway, and associated with reduced p53 accumulation. Our results implicate that EGCG could suppress MG‐induced apoptosis. Support or Funding Information This study was supported by NSC 100‐2313‐B‐309‐003 to A‐C Cheng This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .