Abstract
It has been reported that epigallocatechin-3-gallate(EGCG) could improve cognitive functions in animal models of Alzheimer's disease, but the underlying mechanisms are not completely understood. In order to investigate the effects of EGCG on amyloid-β(Aβ) metabolism and its mechanisms, APP and its proteolytic products were determined by Western blotting and ELISA methods after incubation of N2a/Swe cells with EGCG for 24 h. The results showed that EGCG treatment significantly decreased the levels of Aβ40 and Aβ42 secreted in N2a/Swe cells. Additionally, there was no significant change in APP level after EGCG treatment. Treatment of EGCG dramatically reduced the mRNA and protein expression levels of BACE1. Moreover, EGCG treatment resulted in a reduction of protein level of sAPPβ, an APP fragment cleavaged by BACE1. These results suggest that EGCG inhibits the transcription and translation of BACE1,suppresses the activity of BACE1, and ultimately attenuates Aβ generation, which provides a novel mechanism for the regulation of Aβ metabolism by EGCG.
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