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- W1578492096 endingPage "9717" @default.
- W1578492096 startingPage "9701" @default.
- W1578492096 abstract "Prion diseases caused by aggregated misfolded prion protein (PrP) are transmissible neurodegenerative disorders that occur in both humans and animals. Epigallocatechin-3-gallate (EGCG) has preventive effects on prion disease; however, the mechanisms related to preventing prion diseases are unclear. We investigated whether EGCG, the main polyphenol in green tea, prevents neuron cell damage induced by the human prion protein. We also studied the neuroprotective mechanisms and proper signals mediated by EGCG. The results showed that EGCG protects the neuronal cells against human prion protein-induced damage through inhibiting Bax and cytochrome c translocation and autophagic pathways by increasing LC3-II and reducing and blocking p62 by using ATG5 small interfering (si) RNA and autophagy inhibitors. We further demonstrated that the neuroprotective effects of EGCG were exhibited by a class III histone deacetylase; sirt1 activation and the neuroprotective effects attenuated by sirt1 inactivation using sirt1 siRNA and sirtinol. We demonstrated that EGCG activated the autophagic pathways by inducing sirt1, and had protective effects against human prion protein-induced neuronal cell toxicity. These results suggest that EGCG may be a therapeutic agent for treatment of neurodegenerative disorders including prion diseases." @default.
- W1578492096 created "2016-06-24" @default.
- W1578492096 creator A5007359456 @default.
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- W1578492096 creator A5072096842 @default.
- W1578492096 creator A5080323884 @default.
- W1578492096 date "2015-04-14" @default.
- W1578492096 modified "2023-10-02" @default.
- W1578492096 title "EGCG-mediated autophagy flux has a neuroprotection effect via a class III histone deacetylase in primary neuron cells" @default.
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- W1578492096 doi "https://doi.org/10.18632/oncotarget.3832" @default.
- W1578492096 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4496391" @default.
- W1578492096 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25991666" @default.
- W1578492096 hasPublicationYear "2015" @default.