RESUMEN
Aim To explore mechanism of epigallocatechin-3-gallate (EGCG) on alleviation of hippocampal neuronal autophagy in APP/PSI transgenic mice. Methods 8-month old APP/PSI transgenic mice were randomly divided into three groups;model group (Tg), EGCG low dose group (Tg/EGCG-L), high dose group (Tg/EGCG-H). C57BL/6J mice were utilized as control. Learning and memory were detected by Morris water maze test. The hippocampal ULK1, P62, LC3 I I / LC3 I,mT0R and Aß M2 expressions were detected by Western blot, immunohistochemical staining and ELISA. Results Compared with NT mice, Tg mice showed a marked prolongation of the escape latency in MWM test (P <0. 05). Decreased ULK1 expression and increased P62, LC3 II/LC3 I and A ßM 2 were detected (P < 0. 05). EGCG-treated group showed marked improvement of all these abnormal changes (P < 0. 05). Conclusions EGCG treatment is able to improve cognitive function, which may be attributed to ameliorated autophagic networks dysfunction and reduced Aß plaques in the the hippocampi of APP/PS1 transgenic mice.