Epigallocatechin-3-gallate attenuates impairment of learning and memory in chronic unpredictable mild stress-treated rats by restoring hippocampal autophagic flux.
Epigallocatechin-3-gallate attenuates impairment of learning and memory in chronic unpredictable mild stress-treated rats by restoring hippocampal autophagic flux.
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DOI：
10.1371/journal.pone.0112683
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Liao DF
中科院分区：
文献类型：
--
作者：
Gu HF;Nie YX;Tong QZ;Tang YL;Zeng Y;Jing KQ;Zheng XL;Liao DF
表没食子儿茶素没食子酸酯（Epigallocatechin gallate，EGCG）是绿色茶中的一种主要多酚类物质，对学习和记忆障碍具有有益作用。自噬是一种保护神经元免受应激条件影响的细胞过程。本研究旨在探讨表没食子儿茶素没食子酸酯（EGCG）是否可以挽救慢性不可预测的轻度应激（CITS）诱导的大鼠认知功能障碍，以及其保护作用是否涉及改善自噬通量。正如预期的那样，我们的研究结果表明，BLOTS显着损害记忆能力和抑制自噬通量所示的LC 3-II和p62蛋白水平升高。与此同时，我们观察到增加的神经元损失和激活的哺乳动物雷帕霉素靶蛋白（mTOR）/p70核糖体蛋白S6激酶（p70 S6 k）信号在CA 1区。有趣的是，用EGCG（25 mg/kg，i. p.）显著改善了这些行为改变，减轻了海马CA 1区的组织病理学异常，降低了淀粉样蛋白β 1 -42（Aβ1 - 42）水平，并恢复了自噬通量。然而，阻断自噬通量与氯喹，自噬通量的抑制剂，逆转这些影响的表没食子儿茶素。综上所述，这些发现表明，受损的自噬在CA 1区的CANS大鼠可能有助于学习和记忆障碍。因此，我们得出结论，EGCG的减轻CNS诱导的学习和记忆障碍可能是通过拯救自噬流量。
Epigallocatechin gallate (EGCG) is a major polyphenol in green tea with beneficial effects on the impairment in learning and memory. Autophagy is a cellular process that protects neurons from stressful conditions. The present study was designed to investigate whether EGCG can rescue chronic unpredictable mild stress (CUMS)-induced cognitive impairment in rats and whether its protective effect involves improvement of autophagic flux. As expected, our results showed that CUMS significantly impaired memory performance and inhibited autophagic flux as indicated by elevated LC3-II and p62 protein levels. At the same time, we observed an increased neuronal loss and activated mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6k) signaling in the CA1 regions. Interestingly, chronic treatment with EGCG (25 mg/kg, i.p.) significantly improved those behavioral alterations, attenuated histopathological abnormalities in hippocampal CA1 regions, reduced amyloid beta1–42 (Aβ1−42) levels, and restored autophagic flux. However, blocking autophagic flux with chloroquine, an inhibitor of autophagic flux, reversed these effects of EGCG. Taken together, these findings suggest that the impaired autophagy in CA1 regions of CUMS rats may contribute to learning and memory impairment. Therefore, we conclude that EGCG attenuation of CUMS-induced learning and memory impairment may be through rescuing autophagic flux.
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影响因子：
3.5
作者：
Chen, Di;Pamu, Sreedhar;Cui, Qiuzhi;Chan, Tak Hang;Dou, Q. Ping
通讯作者：
Dou, Q. Ping
影响因子：
5.4
作者：
Nassif M;Hetz C
通讯作者：
Hetz C
慢性应激加剧了tau病理学，神经退行性变化和认知性能，通过伴皮质激素释放因子受体受体依赖性机制在tauopathy的转基因小鼠模型中。
DOI：
10.1523/jneurosci.3836-11.2011
发表时间：
2011-10-05
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Carroll JC;Iba M;Bangasser DA;Valentino RJ;James MJ;Brunden KR;Lee VM;Trojanowski JQ
通讯作者：
Trojanowski JQ
影响因子：
4.8
作者：
Lim, Junghyun;Lee, Yunsu;Oh, Young J.
通讯作者：
Oh, Young J.
影响因子：
2.9
作者：
Rezai-Zadeh, Kavon;Arendash, Gary W.;Tan, Jun
通讯作者：
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