基于脂质组学的EPA调节帕金森病细胞模型 脂代谢的作用研究
Lipidomic-Based Investigation of EPA-Mediated Modulation of Lipid Metabolism in a Cellular Model of Parkinson’s Disease
DOI: 10.12677/acm.2026.1641442, PDF,    科研立项经费支持
作者: 范嘉瑞*, 毛胜敏, 李昱辰, 白群华#:重庆医科大学公共卫生学院,重庆;唐 勇:重庆市中医骨科医院门诊部,重庆
关键词: 帕金森病二十碳五烯酸脂质组学SH-SY5Y细胞线粒体自噬Parkinson’s Disease Eicosapentaenoic Acid Lipidomics SH-SY5Y Cells Mitophagy
摘要: 目的:本研究旨在探讨二十碳五烯酸(Eicosapentaenoic acid, EPA)对帕金森病(Parkinson’s disease, PD)体外模型的神经保护作用,及EPA在神经细胞脂质代谢途径中的潜在保护机制。方法:通过鱼藤酮(Rotenone)干预建立PD体外模型,将人神经母瘤细胞(SH-SY5Y)分为四组培养24 h:对照组(CON组)、模型组(Rotenone组)、治疗组(Rotenone + EPA组)、EPA组,每组进行6次生物重复。24 h培养结束后进行以下处理:通过CCK-8试剂测定每组细胞活力;利用透射电镜(TEM)观察处理后的细胞超微结构变化;将四组细胞收集后进行高分辨率非靶向脂质组相对定量测定,分析EPA对PD神经细胞脂质代谢的影响。结果:EPA可显著提高模型组的细胞活率,并恢复脑源性神经营养因子BDNF、胶质细胞源性神经营养因子GDNF的mRNA表达水平;EPA改善PD模型神经细胞中的线粒体自噬;EPA使PD神经细胞中的脂质代谢谱发生显著变化。结论:EPA对鱼藤酮诱导的PD细胞模型具有神经保护作用,通过改善其脂质代谢紊乱增强对神经细胞膜的稳定性。
Abstract: Objective: This study aims to explore the neuroprotective effect of Eicosapentaenoic acid (EPA) on an in vitro model of Parkinson’s disease (PD), as well as the potential protective mechanism of EPA in the lipid metabolism pathways of nerve cells. Methods: A PD in vitro model was established through Rotenone intervention. Human neuroblastoma cells (SH-SY5Y) were divided into four groups and cultured for 24 hours: control group (CON group), model group (Rotenone group), treatment group (Rotenone + EPA group), and EPA group. Biological replicates were performed in each group six times. After the 24-hour culture was completed, the following treatments were carried out: The viability of each group of cells was determined by CCK-8 reagent; The ultrastructural changes of the treated cells were observed by transmission electron microscopy (TEM). The four groups of cells were collected and subjected to high-resolution non-targeted relative quantitative determination of lipids to analyze the effect of EPA on lipid metabolism in PD nerve cells. Result: EPA could significantly increase the cell viability of the model group and restore the mRNA expression levels of brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF). EPA improves mitochondrial autophagy in nerve cells of the PD model; EPA causes significant changes in the lipid metabolism profile of PD nerve cells. Conclusion: EPA has a neuroprotective effect on rotenone-induced PD cell models, enhancing the stability of nerve cell membranes by improving lipid metabolism disorders.
文章引用:范嘉瑞, 唐勇, 毛胜敏, 李昱辰, 白群华. 基于脂质组学的EPA调节帕金森病细胞模型 脂代谢的作用研究[J]. 临床医学进展, 2026, 16(4): 1991-2001. https://doi.org/10.12677/acm.2026.1641442

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