HO-1 mediated by PI3K/Akt/Nrf2 signaling pathway is involved in (-)-epigallocatechin-3-gallate-rescueing impaired cognitive function induced by chronic cerebral hypoperfusion in rat model

作者全名："Deng, Yu; Zhang, Xiong; Chen, Fei; Huang, Jie; Zhang, Daijiang; Luo, Jie"

作者地址："[Deng, Yu; Chen, Fei; Huang, Jie; Zhang, Daijiang; Luo, Jie] Chongqing Mental Hlth Ctr, Dept Geratol, Chongqing 400000, Peoples R China; [Zhang, Xiong] Chongqing Med Univ, Neurosci Res Ctr, Chongqing, Peoples R China"

通信作者："Deng, Y; Luo, J (通讯作者)，Chongqing Mental Hlth Ctr, Dept Geratol, Chongqing 400000, Peoples R China."

来源：EXPERIMENTAL AGING RESEARCH

ESI学科分类：NEUROSCIENCE & BEHAVIOR

WOS号：WOS:000738507300001

JCR分区：Q4

影响因子：1.8

年份：2022

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期号：　

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结束页：　

文献类型：Article; Early Access

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摘要："Background Epigallocatechin-3-gallate (EGCG) has neuroprotection on chronic cerebral hypoperfusion (CCH) against oxidative stress. HO-1 may represent a target for treatment with CCH. This study aimed to observe the effect of EGCG on cognition impaired in a rat model with CCH and investigate the mechanism. Methods Sprague-Dawley rat models of CCH were established using the 2-VO procedures. Novel object recognition and Morris water maze tests were determined the effects of EGCG on the impaired cognitive functions; HE staining was for detecting the histopathological changes; oxidative stress was assessed by measuring MDA, SOD levels and HO-1 activity. Western blots were for the expression of HO-1, PI3K, Akt (p-Akt), and Nrf2. Results After EGCG treatment, the rats with CCH by 2-VO spent obviously longer time exploring the novel objects, had significantly shorter escape latency and better spatial exploring ability. Meanwhile, EGCG reduced the histopathological changes. Moreover, EGCG increased the concentration of SOD and the activity of HO-1, but decreased the MDA contents. Furthermore, EGCG treatment induced the expression of PI3K, p-Akt, Nrf2, and HO-1 protein, and they were partly reversed by the LY294002, siRNA-Nrf2, or ZnPP. Conclusions EGCG has a neuroprotective effect on rat impaired cognition induced by CCH, possibly by modulating the PI3K/AKT/Nrf2/HO-1 pathway."

基金机构：Natural Science Foundation of Chongqing [cstc2019jcyj-msxmX0673]

基金资助正文：This work was supported by the Natural Science Foundation of Chongqing (cstc2019jcyj-msxmX0673).