Cryptotanshinone protects primary rat cortical neurons from glutamate-induced neurotoxicity via the activation of the phosphatidylinositol 3-kinase/Akt signaling pathway.

Zhang F; Zheng W; Pi R; Mei Z; Bao Y; Gao J; Tang W; Chen S; Liu P

首页> 外文期刊>Experimental Brain Research >Cryptotanshinone protects primary rat cortical neurons from glutamate-induced neurotoxicity via the activation of the phosphatidylinositol 3-kinase/Akt signaling pathway.

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Cryptotanshinone protects primary rat cortical neurons from glutamate-induced neurotoxicity via the activation of the phosphatidylinositol 3-kinase/Akt signaling pathway.

机译：隐丹参酮可通过激活磷脂酰肌醇3激酶/ Akt信号通路保护原代大鼠皮质神经元免受谷氨酸诱导的神经毒性。

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Excitotoxicity contributes to neuronal death and is involved in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD). In the present study, cryptotanshinone, an active ingredient from a Chinese plant, Salvia miltiorrhiza, was investigated to assess its neuroprotective effects against glutamate-induced toxicity in primary culture of rat cortical neurons. Cryptotanshinone reversed glutamate-induced neuronal toxicity, which was characterized by decreased cell viability, increased lactate dehydrogenase release, neuronal DNA condensation, and the alteration of the expression of Bcl-2 family proteins. The neuroprotective effects of cryptotanshinone could be blocked by LY294002 and wortmannin, two inhibitors of PI3K. The importance of the PI3K pathway was further confirmed by the activation of Akt and anti-apoptotic Bcl-2 by cryptotanshinone in a PI3K-dependent manner. These results suggest that cryptotanshinone protects primary cortical neurons from glutamate-induced neurotoxicitythrough the activation of PI3K/Akt pathway. Such neuroprotective effects may be of interest in AD and other neurodegenerative diseases.

机译：兴奋毒性会导致神经元死亡，并参与神经退行性疾病（例如阿尔茨海默氏病（AD））的发病机理。在本研究中，研究了来自中国植物丹参丹参的活性成分隐丹参酮，以评估其对大鼠皮质神经元原代培养物中谷氨酸诱导的毒性的神经保护作用。隐丹参酮逆转谷氨酸诱导的神经元毒性，其特征是细胞活力降低，乳酸脱氢酶释放增加，神经元DNA缩合和Bcl-2家族蛋白表达的改变。隐丹参酮的神经保护作用可以被两种PI3K抑制剂LY294002和渥曼青霉素阻断。通过隐丹参酮以PI3K依赖性方式激活Akt和抗凋亡Bcl-2，进一步证实了PI3K途径的重要性。这些结果表明，隐丹参酮可通过激活PI3K / Akt途径保护原代皮质神经元免受谷氨酸诱导的神经毒性。这种神经保护作用在AD和其他神经退行性疾病中可能是令人感兴趣的。

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来源
《Experimental Brain Research》 |2009年第1期|共10页
作者
Zhang F; Zheng W; Pi R; Mei Z; Bao Y; Gao J; Tang W; Chen S; Liu P;
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正文语种 eng
中图分类人体生理学;
关键词
Glutamate; cryptotanshinone; neuroprotective effects; Neurotoxicity Syndromes;

机译：谷氨酸;隐丹参酮;神经保护作用;神经毒性综合征;

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专利

1. Cryptotanshinone protects primary rat cortical neurons from glutamate-induced neurotoxicity via the activation of the phosphatidylinositol 3-kinase/Akt signaling pathway. [J] . Zhang F, Zheng W, Pi R, Experimental Brain Research . 2009,第1期

机译：隐丹参酮可通过激活磷脂酰肌醇3激酶/ Akt信号通路保护原代大鼠皮质神经元免受谷氨酸诱导的神经毒性。
2. Hyperoside protects primary rat cortical neurons from neurotoxicity induced by amyloid beta-protein via the PI3K/Akt/Bad/Bcl(XL)-regulated mitochondrial apoptotic pathway. [J] . Zeng KW, Wang XM, Ko H, European Journal of Pharmacology: An International Journal . 2011,第1a3期

机译：Hyperoside通过PI3K / Akt / Bad / Bcl（XL）调节的线粒体凋亡途径，保护原代大鼠皮质神经元免受淀粉样β蛋白诱导的神经毒性。
3. Neuroprotective effects of the synthetic cannabinoid HU-210 in primary cortical neurons are mediated by phosphatidylinositol 3-kinase/AKT signaling [J] . Francisco Molina-Holgado, Emmanuel Pinteaux, Laura Heenan, Molecular and cellular neurosciences . 2005,第1期

机译：合成大麻素HU-210在原代皮层神经元中的神经保护作用是由磷脂酰肌醇3-激酶/ AKT信号传导介导的
4. A temporal proteomic analysis of BDNF signaling in primary cortical neurons using SILAC [C] . Guoan Zhang, Pawel Sadowski, Katrin Deihardt, American Society for Mass Spectrometry Conference on Mass Spectrometry and Allied Topics . 2012

机译：硅胶原发性皮质神经元中BDNF信号的时间蛋白质组学分析
5. Role of the phosphatidylinositol (PI) 3-kinase/Akt protein kinase signaling pathway in the survival of rat sympathetic neurons [D] . Crowder, Robert J. 2000

机译：磷脂酰肌醇（PI）3-激酶/ Akt蛋白激酶信号通路在大鼠交感神经元存活中的作用
6. Estrogen Receptor Protein Interaction with Phosphatidylinositol 3-Kinase Leads to Activation of Phosphorylated Akt and Extracellular Signal-Regulated Kinase 1/2 in the Same Population of Cortical Neurons: A Unified Mechanism of Estrogen Action [O] . Paolo Mannella, Roberta Diaz Brinton 2006

机译：雌激素受体蛋白与磷脂酰肌醇3-激酶的相互作用导致在同一皮质神经元群体中磷酸化的Akt和细胞外信号调节激酶1/2的激活：雌激素作用的统一机制
7. Estrogen receptor protein interaction with phosphatidylinositol 3-kinase leads to activation of phosphorylated Akt and extracellular signal-regulated kinase 1/2 in the same population of cortical neurons: A unified mechanism of estrogen action [O] . Mannella, Paolo, Brinton, Roberta Diaz 2006

机译：雌激素受体蛋白与磷脂酰肌醇3激酶的相互作用导致在同一皮质神经元群体中磷酸化Akt和细胞外信号调节激酶1/2的活化：雌激素作用的统一机制

Cryptotanshinone protects primary rat cortical neurons from glutamate-induced neurotoxicity via the activation of the phosphatidylinositol 3-kinase/Akt signaling pathway.

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