SH-SY5Y型
氧化应激
活力测定
化学
活性氧
一氧化氮合酶
一氧化氮
丙二醛
谷胱甘肽
神经保护
超氧化物歧化酶
药理学
细胞凋亡
肿瘤坏死因子α
生物化学
生物
细胞培养
内分泌学
神经母细胞瘤
酶
遗传学
有机化学
作者
Ying chun Li,Hao Jin,Bo Shang,Cheng Zhao,Li juan Wang,Kai Yang,Xiao zhou He,Qian Tian,Zhao Liang Wang,Junfeng Hui,Yang Li,Yanjun Cao
出处
期刊:Phytomedicine
[Elsevier]
日期:2021-07-01
卷期号:87: 153577-153577
被引量:18
标识
DOI:10.1016/j.phymed.2021.153577
摘要
When redox balance is lost in the brain, oxidative stress can cause serious damage that leads to neuronal loss, in congruence with neurodegenerative diseases. Aucubin (AU) is an iridoid glycoside and that is one of the active constituents of Eucommia ulmoides, has many pharmacological effects such as anti-inflammation, anti-liver fibrosis, and anti-atherosclerosis. The present study aimed to evaluate the inhibitory effects of AU on cell oxidative stress against hydrogen peroxide (H2O2)-induced injury in SH-SY5Y cells in vitro. SH-SY5Y cells were simultaneously treated with AU and H2O2 for 24 h. Cell viability was measured by CCK-8. Additionally, mitochondrial membrane depolarization, reactive oxygen species (ROS) generation, and cell apoptosis were measured by flow cytometry. The results showed that AU can significantly increase the H2O2-induced cell viability and the mitochondrial membrane potential, decrease the ROS generation, malondialdehyde (MDA), and increase glutathione (GSH) contents and the superoxide dismutase (SOD) activity. We also found that H2O2 stimulated the production of nitric oxide (NO), which could be reduced by treatment with AU through inhibiting the inducible nitric oxide synthase (iNOS) protein expression. In H2O2-induced SH-SY5Y cells, the levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) content and cell apoptosis were significantly reduced by AU treatment through nuclear factor E2-related factor 2/hemo oxygenase-1 (Nrf2/HO-1) activation, inhibiting the expression of p-NF-κB/NF-κB and down-regulating MAPK and Bcl-2/Bax pathways. These results indicate that AU can reduce inflammation and oxidative stress through the NF-κB, Nrf2/HO-1, and MAPK pathways.
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