首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Potential protection of 2,3,5,4 '-tetrahydroxystilbene-2-O-beta-D-glucoside against staurosporine-induced toxicity on cultured rat hippocampus neurons
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Potential protection of 2,3,5,4 '-tetrahydroxystilbene-2-O-beta-D-glucoside against staurosporine-induced toxicity on cultured rat hippocampus neurons

机译:潜在的保护2,3,5,4'-β-β-D-葡萄糖苷对培养大鼠海马神经元的毒性孢子诱导的毒性

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The present study explored the effect of 2,3,5,4'-tetrahydroxystilbene-2-O-beta-D-glucoside (THSG) on the staurosporine (STS)-induced toxicity in cultured rat hippocampal neurons. The results showed that administration of 200 mu M of THSG significantly protected against 0.3 mu M of STS-induced apoptosis in cultured rat hippocampal neurons tested by methyl thiazolyl tetrazolium (MTT) and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assays. Furthermore, when the Akt signaling pathway was blocked by LY294002, an inhibitor of Phosphatidyl Inositol 3-kinase (PI3K), the protective effects of THSG against STS-induced neurotoxicity were abrogated. We further examined the involvement of PI3K/Akt signaling pathway in THSG protection against STS-induced cytotoxicity on cultured neurons and found that administration of THSG significantly inhibited the STS-induced decreases in the content of phosphoiylated AKt (p-Akt). Moreover, we found that THSG rescued the down-regulation of B cell lymphoma/lewkmia-2 (Bcl(2)) and pro-caspase-3 (pro-Csp3) caused by STS in the neurons. These results indicate that THSG protect the cultured rat hippocampal neurons against STS-induced cytotoxicity and the PI3K/Akt signaling and mitochondrial apoptotic pathways are involved in the THSG-induced protective effects. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
机译:本研究探讨了2,3,5,4'-四羟基苯乙烯-2-β-D-葡萄糖苷(THSG)对培养的大鼠海马神经元的毒性(STS)诱导的毒性的影响。结果表明,200μm的培养大鼠诱导的大鼠海马神经元(MTT)和末端脱氧核苷酸转移酶介导的DUTP瘤末端标记(TUNEL)测定中的培养大鼠海马神经元的培养大鼠海马神经元中的0.3μm诱导的凋亡凋亡诱导的凋亡诱导的凋亡。此外,当通过294002阻断AKT信号传导途径时,磷脂酰肌醇3-激酶(PI3K)的抑制剂,THSG对STS诱导的神经毒性的保护作用耗尽。我们进一步研究了PI3K / AKT信号通路在培养神经元对STS诱导的细胞毒性中的PI3K / AKT信号传导途径的参与,发现THSG的施用显着抑制STS诱导的磷酸化AKT(P-AKT)的含量降低。此外,我们发现THSG救出了由神经元中的STS引起的B细胞淋巴瘤/ Lewkmia-2(Bcl(2))和Pro-Caspase-3(Pro-CSP3)的下调。这些结果表明,THSG保护培养的大鼠海马神经元免受STS诱导的细胞毒性,并且PI3K / AKT信号传导和线粒体凋亡途径参与THSG诱导的保护作用。 (c)2014 Elsevier Ireland Ltd.保留所有权利。

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