EPA-enriched ethanolamine plasmalogen and EPA-enriched phosphatidylethanolamine enhance BDNF/TrkB/CREB signaling and inhibit neuronal apoptosis in vitro and in vivo.,Food & Function

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EPA-enriched ethanolamine plasmalogen and EPA-enriched phosphatidylethanolamine enhance BDNF/TrkB/CREB signaling and inhibit neuronal apoptosis in vitro and in vivo.
Food & Function ( IF 5.1 ) Pub Date : 2020-02-11 , DOI: 10.1039/c9fo02323b
Hongxia Che ₁ , Lingyu Zhang , Lin Ding , Wancui Xie , Xiaoming Jiang , Changhu Xue , Tiantian Zhang , Yuming Wang

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Our previous study showed that EPA-enriched ethanolamine plasmalogen (EPA-pPE) exerted more significant effects than EPA-enriched phosphatidylethanolamine (EPA-PE) in improving learning and memory deficit. However, the results of the mechanism study were not consistent with the improved cognitive function, which suggested that other signaling pathways might be involved. In the present study, primary cultured hippocampal neurons and cognitive deficiency rats were used to compare the effects of EPA-pPE and EPA-PE on brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB)/cAMP response element-binding protein (CREB) signaling and neuronal apoptosis. The in vitro experiment showed that both EPA-pPE and EPA-PE could relieve cell death and improve the cellular morphology of neurons via upregulating anti-apoptotic proteins and downregulating pro-apoptotic proteins. The in vivo experiment showed that EPA-pPE exerted more significant effects than EPA-PE in improving the number of neuronal Nissl bodies, increasing the branching of dendrites and dendritic spine density in cortical neurons, as well as improving the expression of synaptic vesicle-related proteins synaptophysin (SYN) and PSD95 via BDNF/TrkB/CREB signaling. These results indicated that EPA-pPE exerted neuroprotection at least partly through inhibiting neuronal apoptosis and enhancing the BDNF/TrkB/CREB pathway, which suggests that EPA-enriched plasmalogen can be explored as a potential therapeutic agent in long-term Alzheimer's disease therapy.

中文翻译：

富含 EPA 的乙醇胺缩醛磷脂和富含 EPA 的磷脂酰乙醇胺可在体外和体内增强 BDNF/TrkB/CREB 信号传导并抑制神经元凋亡。

我们之前的研究表明，富含 EPA 的乙醇胺缩醛磷脂 (EPA-pPE) 在改善学习和记忆缺陷方面比富含 EPA 的磷脂酰乙醇胺 (EPA-PE) 具有更显着的效果。然而，机制研究的结果与认知功能的改善并不一致，这表明可能涉及其他信号通路。本研究利用原代培养的海马神经元和认知缺陷大鼠，比较EPA-pPE和EPA-PE对脑源性神经营养因子（BDNF）/原肌球蛋白受体激酶B（TrkB）/cAMP反应元件结合的影响蛋白（CREB）信号传导和神经元凋亡。体外实验表明，EPA-pPE和EPA-PE均可以通过上调抗凋亡蛋白和下调促凋亡蛋白来缓解细胞死亡并改善神经元的细胞形态。体内实验表明，EPA-pPE在提高神经元尼氏小体数量、增加皮层神经元树突分枝和树突棘密度、提高突触小泡相关蛋白表达等方面比EPA-PE具有更显着的效果。通过 BDNF/TrkB/CREB 信号转导蛋白突触素 (SYN) 和 PSD95。这些结果表明，EPA-pPE至少部分通过抑制神经元凋亡和增强BDNF/TrkB/CREB途径发挥神经保护作用，这表明富含EPA的缩醛磷脂可以作为长期阿尔茨海默病治疗的潜在治疗剂。

更新日期：2020-02-26

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