Fucoxanthin prevents H(2)O(2)-induced neuronal apoptosis via concurrently activating the PI3-K/Akt cascade and inhibiting the ERK pathway.
Fucoxanthin prevents H(2)O(2)-induced neuronal apoptosis via concurrently activating the PI3-K/Akt cascade and inhibiting the ERK pathway.
复制标题
岩藻黄质通过同时激活 PI3-K/Akt 级联和抑制 ERK 通路来防止 H2O2 诱导的神经元凋亡
DOI：
10.1080/16546628.2017.1304678
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发表时间：
2017
影响因子：
3.3
通讯作者：
Zhang JR
中科院分区：
文献类型：
--
作者：
Yu J;Lin JJ;Yu R;He S;Wang QW;Cui W;Zhang JR
摘要背景：岩藻黄质是一种富含于褐藻叶绿体中的天然类胡萝卜素，具有多种保健功能，尤其是抗氧化作用。目的：研究岩藻黄素对过氧化氢（H2 O2）诱导的神经元凋亡的保护作用。设计：以SH-SY 5 Y细胞和原代小脑颗粒神经元为模型，研究岩藻黄素对H2 O2诱导的神经元损伤的保护作用。结果：岩藻黄素对H2 O2诱导的神经元凋亡和细胞内活性氧有明显的保护作用。H2 O2处理导致SH-SY 5 Y细胞磷脂酰肌醇3-激酶（PI 3-K）/Akt级联反应活性降低，细胞外信号调节激酶（ERK）通路活性升高。此外，岩藻黄素显着恢复由H2 O2诱导的PI 3-K/Akt和ERK通路的活性改变。糖原合成酶激酶3β（GSK 3 β）和丝裂原活化蛋白激酶激酶（MEK）的特异性抑制剂对H2 O2诱导的神经元死亡具有显著的保护作用。此外，岩藻黄质对H2 O2诱导的神经元死亡的神经保护作用被特定的PI 3-K抑制剂消除。结论：我们的数据有力地揭示了岩藻黄素通过同时激活PI 3-K/Akt级联和抑制ERK通路来保护H2 O2诱导的神经毒性，为使用岩藻黄素治疗氧化应激诱导的神经退行性疾病提供了支持。
ABSTRACT Background: As a natural carotenoid abundant in chloroplasts of edible brown algae, fucoxanthin possesses various health benefits, including anti-oxidative activity in particular. Objective: In the present study, we studied whether fucoxanthin protected against hydrogen peroxide (H2O2)-induced neuronal apoptosis. Design: The neuroprotective effects of fucoxanthin on H2O2-induced toxicity were studied in both SH-SY5Y cells and primary cerebellar granule neurons. Results: Fucoxanthin significantly protected against H2O2-induced neuronal apoptosis and intracellular reactive oxygen species. H2O2 treatment led to the reduced activity of phosphoinositide 3-kinase (PI3-K)/Akt cascade and the increased activity of extracellular signal-regulated kinase (ERK) pathway in SH-SY5Y cells. Moreover, fucoxanthin significantly restored the altered activities of PI3-K/Akt and ERK pathways induced by H2O2. Both specific inhibitors of glycogen synthase kinase 3β (GSK3β) and mitogen-activated protein kinase kinase (MEK) significantly protected against H2O2-induced neuronal death. Furthermore, the neuroprotective effects of fucoxanthin against H2O2-induced neuronal death were abolished by specific PI3-K inhibitors. Conclusions: Our data strongly revealed that fucoxanthin protected against H2O2-induced neurotoxicity via concurrently activating the PI3-K/Akt cascade and inhibiting the ERK pathway, providing support for the use of fucoxanthin to treat neurodegenerative disorders induced by oxidative stress.