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An Important Function of Petrosiol E in Inducing the Differentiation of Neuronal Progenitors and in Protecting Them against Oxidative Stress
Advanced Science ( IF 15.1 ) Pub Date : 2017-07-05 , DOI: 10.1002/advs.201700089
Jing Liu 1, 2 , Linlin Wang 1 , Yuguo Du 1, 2 , Sijin Liu 1, 2
Affiliation  

Insufficient endogenous neurotrophin supply contributes to neurodegeneration. Meanwhile, neuronal injuries are also attributed to oxidative stress upon toxin exposure. Thus, reconstruction neurite extension and antioxidative stress are the potential strategies for ameliorating neuronal injuries. However, there is no well‐defined therapeutic developed in this regard. In search of such therapeutics, Petrosiol E is identified here as a potent inducer to guide the differentiation of neuronal progenitor cells. Petrosiol E also considerably promotes embryonic stem cell differentiation into neural ectoderm features. Moreover, Petrosiol E reveals an antioxidant function to protect cells from oxidative stress induced by arsenic. Moreover, the molecular mechanism underlying Petrosiol E‐induced neuronal differentiation is uncovered: (a) enhancement of NF‐E2‐related factor 2 (Nrf 2) activity in driving neuronal differentiation; (b) diminishment of oxidative stress. Petrosiol E activates the mitogen‐activated protein kinase and serine/threonine kinase signaling to enhance the activity of Nrf 2. As a result of enhanced Nrf 2 activity, neuronal differentiation is accelerated, and the cellular antioxidation responses are also enforced, even under arsenic‐induced neurotoxicity. Together, the combined results unveil a desirable role of Petrosiol E in driving neuronal differentiation and in combating oxidative stress. This study would open an avenue to develop new therapeutics based on Petrosiol compounds to treat neurodegenerative diseases.

中文翻译:

Petrosiol E 在诱导神经元祖细胞分化和保护它们免受氧化应激方面的重要功能

内源性神经营养素供应不足会导致神经变性。同时,神经元损伤也归因于毒素暴露时的氧化应激。因此,重建神经突延伸和抗氧化应激是改善神经元损伤的潜在策略。然而,在这方面还没有开发出明确的治疗方法。在寻找此类疗法的过程中,Petrosiol E 被鉴定为一种有效的诱导剂,可指导神经元祖细胞的分化。Petrosiol E 还显着促进胚胎干细胞分化为神经外胚层特征。此外,Petrosiol E 具有抗氧化功能,可保护细胞免受砷引起的氧化应激。此外,揭示了 Petrosiol E 诱导神经元分化的分子机制:(a)增强 NF-E2 相关因子 2(Nrf 2)驱动神经元分化的活性;(b) 减少氧化应激。Petrosiol E 激活丝裂原激活蛋白激酶和丝氨酸/苏氨酸激酶信号传导以增强 Nrf 2 的活性。由于 Nrf 2 活性增强,神经元分化加速,细胞抗氧化反应也得到加强,即使在砷作用下也是如此。诱发的神经毒性。总之,综合结果揭示了 Petrosiol E 在驱动神经元分化和对抗氧化应激方面的理想作用。这项研究将为开发基于 Petrosiol 化合物的新疗法来治疗神经退行性疾病开辟一条途径。
更新日期:2017-07-05
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