Orexin-A protects SH-SY5Y cells against H(2)O(2)-induced oxidative damage via the PI3K/MEK(1/2)/ERK(1/2) signaling pathway.
Orexin-A protects SH-SY5Y cells against H(2)O(2)-induced oxidative damage via the PI3K/MEK(1/2)/ERK(1/2) signaling pathway.
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Orexin-A 通过 PI3K/MEK1/2/ERK1/2 信号通路保护 SH-SY5Y 细胞免受 H2O2 诱导的氧化损伤
DOI:
10.1177/2058738418785739
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发表时间:
2018-01
影响因子:
3.5
通讯作者:
Bai B
中科院分区:
文献类型:
--
作者:
Wang CM;Yang CQ;Cheng BH;Chen J;Bai B
Orexin-A elicits multiple potent effects on a variety of tumor cells via different signaling pathways. However, it is unknown whether it has a neuroprotective effect on SH-SY5Y human neuroblastoma cells. This study investigated the neuroprotective effect of Orexin-A against hydrogen peroxide (H2O2)-induced oxidative damage in SH-SY5Y cells and the underlying mechanism. H2O2 treatment decreased the viability of SH-SY5Y cells, induced apoptosis, and decreased superoxide dismutase activity. Orexin-A attenuated these effects, indicating that it protects SH-SY5Y cells against H2O2-induced oxidative damage. Pre-treatment with Orexin-A also attenuated H2O2-induced increases in phosphorylation of MEK1/2 and ERK1/2. Moreover, these effects of Orexin-A were reduced in the presence of the PI3K inhibitor LY294002. Finally, pre-treatment with LY294002 abrogated attenuation of the H2O2-induced decrease in cell viability and increase in caspase-3/7 activity by Orexin-A. These results show that the PI3K/MEK1/2/ERK1/2 signaling pathway is involved in the neuroprotective effects of Orexin-A against H2O2-induced oxidative damage in SH-SY5Y cells. Our findings provide insight into the neuroprotective effects of Orexin-A and the underlying mechanism, which will be useful for the treatment of nervous system diseases.
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