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防治邻苯二甲酸二(2-乙基)己酯诱导的 PC12 细胞线粒体功能障碍和细胞凋亡。

Prevents DEHP-Induced Mitochondrial Dysfunction and Apoptosis in PC12 Cells.

机构信息

Laboratory for Research on Biologically Compatible Compounds, Faculty of Dental Medicine, University of Monastir, Rue Avicenne, Monastir 5019, Tunisia.

Department of Biomedical and Biotechnological Sciences, University of Catania, Torre Biologica, Via Santa Sofia n. 97, 95125 Catania, Italy.

出版信息

Int J Mol Sci. 2020 Mar 20;21(6):2138. doi: 10.3390/ijms21062138.

DOI:10.3390/ijms21062138
PMID:32244920
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7139838/
Abstract

(HE) is a medicinal plant known to possess anticarcinogenic, antibiotic, and antioxidant activities. It has been shown to have a protective effect against ischemia-injury-induced neuronal cell death in rats. As an extending study, here we examined in pheochromocytoma 12 (PC12) cells, whether HE could exert a protective effect against oxidative stress and apoptosis induced by di(2-ethylhexyl)phthalate (DEHP), a plasticizer known to cause neurotoxicity. We demonstrated that pretreatment with HE significantly attenuated DEHP induced cell death. This protective effect may be attributed to its ability to reduce intracellular reactive oxygen species levels, preserving the activity of respiratory complexes and stabilizing the mitochondrial membrane potential. Additionally, HE pretreatment significantly modulated Nrf2 and Nrf2-dependent vitagenes expression, preventing the increase of pro-apoptotic and the decrease of anti-apoptotic markers. Collectively, our data provide evidence of new preventive nutritional strategy using HE against DEHP-induced apoptosis in PC12 cells.

摘要

(HE) 是一种药用植物,已知具有抗癌、抗菌和抗氧化活性。它已被证明对大鼠缺血性损伤诱导的神经元细胞死亡具有保护作用。作为一项延伸研究,我们在这里研究了嗜铬细胞瘤 12 细胞 (PC12),HE 是否可以对邻苯二甲酸二(2-乙基己基)酯 (DEHP) 诱导的氧化应激和细胞凋亡发挥保护作用,DEHP 是一种已知具有神经毒性的增塑剂。我们证明,HE 的预处理可显著减轻 DEHP 诱导的细胞死亡。这种保护作用可能归因于它降低细胞内活性氧水平的能力,保持呼吸复合物的活性并稳定线粒体膜电位。此外,HE 预处理还显著调节了 Nrf2 和 Nrf2 依赖性 vitagenes 的表达,防止了促凋亡标志物的增加和抗凋亡标志物的减少。总之,我们的数据提供了使用 HE 对抗 PC12 细胞中 DEHP 诱导的细胞凋亡的新的预防营养策略的证据。

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