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食欲素 A 通过 PI3K/MEK/ERK 信号通路对 HO 诱导的 SH-SY5Y 细胞氧化损伤起保护作用。

Orexin-A protects SH-SY5Y cells against HO-induced oxidative damage via the PI3K/MEK/ERK signaling pathway.

机构信息

1 Neurobiology Key Laboratory of Jining Medical University in Colleges of Shandong, Jining, P.R. China.

2 Division of Biomedical Sciences, Warwick Medical School, University of Warwick, Coventry, UK.

出版信息

Int J Immunopathol Pharmacol. 2018 Jan-Dec;32:2058738418785739. doi: 10.1177/2058738418785739.

DOI:10.1177/2058738418785739
PMID:29983082
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6073832/
Abstract

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 (HO)-induced oxidative damage in SH-SY5Y cells and the underlying mechanism. HO 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 HO-induced oxidative damage. Pre-treatment with Orexin-A also attenuated HO-induced increases in phosphorylation of MEK and ERK. 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 HO-induced decrease in cell viability and increase in caspase-3/7 activity by Orexin-A. These results show that the PI3K/MEK/ERK signaling pathway is involved in the neuroprotective effects of Orexin-A against HO-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.

摘要

食欲素-A 通过不同的信号通路对多种肿瘤细胞产生多种强效作用。然而，目前尚不清楚它是否对 SH-SY5Y 人神经母细胞瘤细胞具有神经保护作用。本研究探讨了食欲素-A 对 SH-SY5Y 细胞过氧化氢 (HO) 诱导的氧化损伤的神经保护作用及其潜在机制。HO 处理降低了 SH-SY5Y 细胞的活力，诱导细胞凋亡，并降低了超氧化物歧化酶的活性。食欲素-A 减弱了这些作用，表明它对 SH-SY5Y 细胞免受 HO 诱导的氧化损伤。预孵育食欲素-A 也减弱了 HO 诱导的 MEK 和 ERK 磷酸化增加。此外，在存在 PI3K 抑制剂 LY294002 的情况下，食欲素-A 的这些作用减少。最后，LY294002 的预处理消除了食欲素-A 对 HO 诱导的细胞活力降低和 caspase-3/7 活性增加的抑制作用。这些结果表明，PI3K/MEK/ERK 信号通路参与了食欲素-A 对 SH-SY5Y 细胞 HO 诱导的氧化损伤的神经保护作用。我们的研究结果为食欲素-A 的神经保护作用及其潜在机制提供了深入了解，这将有助于神经系统疾病的治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/8854847ac867/10.1177_2058738418785739-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/b04c4304f83e/10.1177_2058738418785739-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/4ce507f9ffc3/10.1177_2058738418785739-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/39f8d67e0f8c/10.1177_2058738418785739-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/a0686227b250/10.1177_2058738418785739-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/7e72b0b68ad0/10.1177_2058738418785739-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/8b4de3de535c/10.1177_2058738418785739-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/fe920ddea2b0/10.1177_2058738418785739-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/8854847ac867/10.1177_2058738418785739-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/b04c4304f83e/10.1177_2058738418785739-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/4ce507f9ffc3/10.1177_2058738418785739-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/39f8d67e0f8c/10.1177_2058738418785739-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/a0686227b250/10.1177_2058738418785739-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/7e72b0b68ad0/10.1177_2058738418785739-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/8b4de3de535c/10.1177_2058738418785739-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/fe920ddea2b0/10.1177_2058738418785739-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a69e/6073832/8854847ac867/10.1177_2058738418785739-fig8.jpg

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