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首页> 外文期刊>Journal of cellular physiology. >Cyclo‐glycylproline attenuates hydrogen peroxide‐induced cellular damage mediated by the MDM2‐p53 pathway in human neural stem cells
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Cyclo‐glycylproline attenuates hydrogen peroxide‐induced cellular damage mediated by the MDM2‐p53 pathway in human neural stem cells

机译：环甘氨酰脯氨酸减弱人神经干细胞中MDM2-p53通路介导的过氧化氢诱导的细胞损伤

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Abstract Cyclo‐glycylproline (cGP), a cyclic dipeptide containing a condensation bond between glycine and proline, is produced by the cyclization of the N‐terminal tripeptide of insulin‐like growth factor‐1. Previous studies have shown that cGP administration exerts a neuroprotective effect and enhances the regenerative ability in rats with ischemic brain injury. The efficacy of cGP is medicated by regulating the bioavailability of insulin‐like growth factor‐1 (IGF‐1), however, the molecular mechanisms underlying the neuroprotective effects of cGP on brain damage remains to be elucidated. In the current study, we investigated the cGP‐mediated molecular mechanism in human fetal neural stem cells (hfNSCs) exposed to oxidative stress, which is a key factor affecting the development of several brain diseases, including traumatic brain injury and Parkinson's disease. We found that cGP treatment attenuated oxidative stress‐induced cell death in cultured hfNSCs in a dose‐dependent manner. Transcriptome analysis revealed that under oxidative stress conditions, p53‐mediated signaling was activated, accompanied by upregulation of mouse double minute 2 homolog (MDM2), a p53‐specific E3 ubiquitin ligase, in cGP‐treated hfNSCs. By using a comprehensive protein phosphorylation array, we found that cGP induced the activation of Akt signaling pathway, which enhanced the expression of MDM2, in hfNSCs exposed to oxidative stress. Moreover, the MDM2 inhibitor nutlin‐3 inhibited the protective effect of cGP on oxidative stress‐induced cell death and apoptosis. Therefore, cGP attenuates oxidative stress‐induced cell death mediated by the interplay between IGF‐1 signaling and the MDM2‐p53 pathway in human NSCs. We revealed the molecular mechanism underlying cGP‐induced neuroprotective properties in a model of brain damage.
机译：文摘三轮车glycylproline应承担(本金保证产品),循环二肽债券之间包含一个冷凝甘氨酸和脯氨酸,是产生的环化的N末端三肽等类胰岛素生长因子1。表明,本金保证产品政府施加一个吗神经保护效应,增强了在大鼠缺血性脑再生能力受伤。调节胰岛素的生物利用度等地理地理生长因子1 (IGF 1),然而,分子潜在的神经保护作用机制本金保证产品的脑损伤还有待阐明。在当前的研究中,我们调查了人类胎儿本金保证产品量调节的分子机制神经干细胞(hfNSCs)暴露于氧化压力,这是一个关键因素影响发展一些脑部疾病,包括创伤性脑损伤和帕金森病。我们发现本金保证产品治疗减毒氧化压力在培养hfNSCs诱导细胞死亡剂量依赖的方式。透露,在氧化应激条件下,p53检测介导信号被激活,陪同upregulation鼠标两分钟2同族体地理(MDM2) p53 E3泛素连接酶,本金保证产品检测hfNSCs治疗。蛋白质磷酸化数组,我们发现本金保证产品诱导一种蛋白激酶信号通路的激活,增强MDM2的表达,在hfNSCs吗暴露于氧化应激。抑制剂nutlin 3抑制保护本金保证产品对氧化应激诱导细胞死亡和细胞凋亡。氧化应激诱导细胞死亡的IGF 1信号和应承担的之间的相互作用在人类nsc MDM2检测p53通路。分子机制本金保证产品的诱导神经在大脑的模型属性损害。

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