A comparative study of EPA-enriched ethanolamine plasmalogen and EPA-enriched phosphatidylethanolamine on Aβ₄₂ induced cognitive deficiency in a rat model of Alzheimer's disease

Abstract

Ethanolamine plasmalogen (pPE), a major phospholipid in neuronal membranes, is specifically reduced in postmortem brains from patients with Alzheimer's disease (AD). The purpose of the present study was to compare the effects of EPA-enriched ethanolamine plasmalogen (EPA-pPE) and EPA-enriched phosphatidylethanolamine (EPA-PE) on cognitive deficiency and illustrate the possible underlying mechanisms. SD rats were divided into four groups including the sham group injected with 0.9% saline and three amyloid-β (Aβ) infusion groups, Aβ42 group, EPA-pPE group and EPA-PE group. EPA-pPE and EPA-PE were administered by gavage (150 mg kg-1 day-1), respectively, once a day for 26 days. Administration of EPA-pPE exerted better effects than EPA-PE in improving Aβ-induced cognitive deficiency in a rat model of Alzheimer's disease. Further mechanical research indicated that EPA-pPE was superior to EPA-PE in regulating oxidative stress via increasing SOD activity and decreasing MDA level, as well as reducing GSK-3β and tau phosphorylation. Moreover, EPA-PE was more effective than EPA-pPE at inhibiting the protein expressions of Bax and caspase 9. The results of neuro-inflammation and inflammasome activation showed that EPA-pPE exerted more significant effects than EPA-PE in inhibiting the expressions of TNF-α and IL-1β, and decreasing NLRP3, pro-caspase 1 and caspase 1 levels. EPA-pPE alleviated Aβ-induced neurotoxicity by inhibiting oxidative stress, neuronal injury, apoptosis and neuro-inflammation, which might depend on the vinyl ether linkage at the sn-1 position.

Cerebrosides from Sea Cucumber Improved Aβ1–42‐Induced Cognitive Deficiency in a Rat Model of Alzheimer's Disease

“…Previous studies have suggested that Alzheimer's disease is directly or indirectly related to neuronal apoptosis . Our previous studies demonstrated that intracerebroventricular injection of A β 1–42 caused neuronal apoptosis . What is more, previous study showed that cerebrosides isolated from the seeds of S. lychnophora could protect SH‐SY5Y cell against damage induced by hydrogen peroxide .…”

Oral administration of a synthetic vinyl-ether plasmalogen normalizes open field activity in a mouse model of rhizomelic chondrodysplasia punctata

“…Natural sources of plasmalogen are not readily available, and thus dietary approaches to increase plasmalogen deficiency in RCDP are not feasible. Plasmalogen extracts have been generated from animal and marine tissues and tested in rodent models of Alzheimer's disease (Che et al, 2018;Hossain et al, 2018;Sejimo et al, 2018;Yamashita et al, 2017) and human patients with mild Alzheimer's disease (Fujino et al, 2017). The animal studies showed an improvement in the cognitive impairment and reduction in the neuroinflammation associated with Alzheimer's disease.…”

Dietary PlsEtn Ameliorates Colon Mucosa Inflammatory Stress and ACF in DMH‐Induced Colon Carcinogenesis Mice: Protective Role of Vinyl Ether Linkage

“…We have shown that the extrinsic supply of PlsEtn bearing n‐3 PUFA suppresses neuronal apoptosis through the mitochondrial pathway and improves impaired memory in a rat model of AD (Yamashita et al, 2015, 2016a, 2017a). In addition, EPA‐enriched PlsEtn rather than EPA‐enriched PtdEtn alleviated amyloid β‐induced neurotoxicity by inhibiting oxidative stress, neural injury, apoptosis, and neuro‐inflammation, which depended on the vinyl ether linkage in the sn ‐1 position (Che et al, 2018). However, the functional role of dietary PlsEtn in the health of intestines remains unknown.…”

“…In light of the demonstrated superiority of PlsEtn over PtdEtn in neuroprotective functions (Che et al, 2018) and the relationship of PlsEtn levels and a dysfunction in the colon mucosa (Lopez et al, 2018) as aforementioned, we hypothesized that dietary intake of PlsEtn may suppress colon inflammatory stress and subsequent formation of colon precancerous lesions (aberrant crypt foci – ACF) possibly due to a high presence of alkenyl (vinyl ether) linkages. In the present study, we elucidated the effect of diets supplemented with purified EtnGpl consisting of high and low PlsEtn ratios on the formation of ACF using a 1,2‐dimethylhydrazine (DMH)‐induced colon carcinogenesis mice model.…”