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The DHA/EPA enriched ethanolamine plasmalogens (EPA-PlsEtn) are widely present in seafood, and EPA-PlsEtn exhibits unique effects on improving cognitive functions. However, there were no reports on the alleviation of dietary EPA-PlsEtn on atherosclerosis. In the present study, supplementation with EPA-PlsEtn for 8 weeks dramatically reduced atherosclerotic lesions by 78% and serum LDL-c levels by 73.9% compared with model group. EPA-PlsEtn possessed lowest hepatic cholesterol levels associated with increased bile acids synthesis and excretion into feces. EPA-PlsEtn increased CYP7A1 expression through suppressing FXR activation. The increased proportion of bile acid TMCA, FXR antagonist, might contribute to the increased bile acid synthesis. In conclusion, different with EPA in form of EE or PC, EPA-PlsEtn efficiently alleviated atherosclerosis via lowering cholesterol levels by suppressing FXR expression. These findings provided new evidence and thought to explain the unique bioactivity of EPA-PlsEtn and new sight to re-understand the structure-activities relationship of DHA/EPA.

Eicosapentaenoic acid (EPA) enriched phospholipids (EPA-PL) are widely distributed in marine products. It has been reported that the protective effects of the mixture of EPA and docosahexaenoic acid (DHA) on Parkinson’s disease (PD), however, it is hard to confirm the improvement of EPA alone on PD. In the present study, EPA-PL was extracted from the sea cucumber (Cucumaria frondosa) to compare the effects of EPA-PL and commercial EPA in the form of ethyl ester (EPA-EE) on PD mice induced by 1-methyl-4-phenyl-1,2,3,6 -tetrahydropyridine (MPTP). Results showed that dietary EPA-PL instead of EPA-EE notably improved MPTP-induced behavioral deficiency. Further research showed that EPA-PL suppressed MPTP-induced oxidative stress and apoptosis, thereby alleviating the loss of dopaminergic neurons via mitochondria – mediated pathway and mitogen-activated protein kinase pathway. These findings firstly confirmed that EPA-PL could improve MPTP-induced symptoms and pathology of PD, providing a reference for the prevention and treatment of neurodegenerative diseases.

Docosahexaenoic acid (DHA) enriched phospholipids such as phosphatidylcholine (PC) and phosphatidylserine (PS) are important bioactive components and widely distributed in multifarious marine products. In the present study, we investigated the effects of DHA enriched phospholipids with different polar groups (DHA-PC and DHA-PS) on MPTP-induced PD mice by behavioral experiments including rotarod test and open field test as well as immunohistochemistry. Three DHA supplements all exhibited observable protective effects on PD symptoms of MPTP-induced mice and increased the number of dopaminergic neurons, especially DHA-PS had better improvement than DHA-TG and DHA-PC. Further analysis indicated that DHA additive pretreatment could inhibit apoptosis via mitochondria - mediated pathway and MAPK pathway, and thus protecting dopaminergic neurons in MPTP-induced mice. These results suggested that DHA enriched phospholipids with different polar groups exerted varying improvements on MPTP-induced PD mice, which represented a potential novel therapeutic candidate for the prevention and treatment of neurodegenerative diseases.

EPA enriched ethanolamine plasmalogens (EPA-pPE) are important bioactive components and widely distributed in multifarious marine products. In the present study, Chinese hamster ovary cells stably transfected with APP751 and PS1 (CHO-APP/PS1 cells) and high-fat feeding SAMP8 mice were used to study the effects of EPA-pPE on Alzheimer’s disease (AD). The in vitro experiments showed that EPA-pPE exerted better effects than EPA-PE and Egg-PE in decreasing the intracellular and extracellular Aβ levels. EPA-pPE obviously improved learning and memory function of high-fat feeding SAMP8 mice by Morris maze test. Further mechanism research indicated that EPA-pPE could significantly improve cognition of Alzheimer’s disease by suppressing β-amyloid generation via reducing levels of APP and altering APP cleavage, thereby inhibiting oxidative stress, hyper-phosphorylated tau, neuro-inflammation and apoptosis. These results suggested that EPA-pPE might be applied as food supplements and/or functional ingredients to relieve neurodegenerative disease.

Gangliosides (GLSs), abundant in the mammalian brain, have been shown to affect neuronal plasticity and neurodegenerative diseases, especially Alzheimer’s disease. However, the biological activity and neuroprotective mechanism have not yet been established for sea urchin GLSs (SU-GLSs). Herein, we evaluated the neuroprotective effect of Strongylocentrotus nudus GM4(1S), GD4(1S), GD4(2A), and GD4(2G) in Aβ25-35-induced PC12 cells and in vivo using a GLSs mixture administered to SAMP8 mice. It was established that the pre-treatment of SU-GLSs decreased the loss of cell viability and the levels of Aβ1-40 and Aβ1-42 in the hippocampus significantly, and relieved the cognitive deficiency of SAMP8 mice. Mechanistic studies found that SU-GLSs down regulated the expression of Bax, Caspase-3, and Caspase-9, while it upregulated the expression of Bcl-2, synaptophysin, and GAP-43 significantly. Thus, SU-GLSs promoted resistance to AD in a dose-dependent and structure-selective manner, probably via reducing the loss of neurites and blocking the mitochondrial apoptosis pathway.

Dietary fish oil could prevent and treat atherosclerosis by improving lipid metabolism; in apolipoprotein E-deficient (apoE −/− ) mice, it was ineffective at lowering serum lipid levels but still showed anti-atherosclerosis action. To date, no direct evidence has comparatively evaluated the effect of docosahexaenoic acid-enriched and eicosapentaenoic acid-enriched phospholipids (DHA-PL and EPA-PL) on atherosclerosis in apoE −/− mice. The present study suggested that both 1% dietary DHA-PL and EPA-PL could significantly reduce atherosclerotic lesions (37.4% and 53.4%, respectively) in high fat diet apoE −/− mice. EPA-PL significantly decreased serum and hepatic lipid levels, by mediating mRNA and protein levels of genes related to hepatic cholesterol metabolism, whereas DHA-PL was ineffective. In the suppression of aortic proinflammatory cytokines, DHA-PL was superior to EPA-PL at reducing TNF-α, IL-6, and IL-1β transcription. In conclusion, the action of DHA-PL was simply anti-inflammatory, and that of EPA-PL was mainly the improvement of lipid metabolism in the amelioration of atherosclerosis.

Recent study demonstrated that dietary eicosapentaenoic acid (EPA) could alleviate metabolism disorders. However, the onset time of EPA-enriched phospholipid (EPA-PL) on lipid metabolism was rarely been reported. The aim of the present study was to evaluate the time-dependent changes in lipid profile and genes of lipometabolism induced by EPA-PL from Cucumaria frondosa. Male C57BL/6J mice were fed a standard diet with or without EPA-PL for 3, 7, or 14 days. Additionally, we examined gene expression 1 week after removing EPA-PL from the diet. Our results indicated that 3-day EPA-PL supplementation significantly increased the expression of genes related to β-oxidation (UCP2, Ehhadh, Acaa1) in the liver and epididymal adipose tissue, whereas no differences were observed in the mRNA expression of selected genes between groups 1 week after EPA-PL removal. It is concluded that EPA-PL served as a rapid regulator of fat burning and could be a functional food for obesity disorders.

Echinoside A (EA) and holothurin A (HA) are the major saponins found in sea cucumbers. Their pharmacokinetics were studied following intravenous and oral administration of saponin extracts in rats. The serum and liver of rat were pretreated by protein precipitation and performed on ENVI-18 SPE cartridges. The compounds were analyzed by using a high-performance liquid chromatography–mass spectrometry (HPLC-MS) method in the single ion monitoring (SIM) mode. The results demonstrated that serum EA concentration rapidly reduced in 5 min after intravenous administration. HA serum concentration reduced to its lowest level after 1 h. After oral administration, EA reached its peaks at 3 h and 7 h. The first peak of HA occurred at 3 h and reached a second peak at 9 h. In the liver, there were two peaks for EA at 2 h and 9 h, and only one peak for HA at 9 h.

Abundant studies have proven that the protective effects of omega-3 polyunsaturated fatty acids enriched phospholipids (n-3 PUFA-PLs) mainly derived from fish roe and Antarctic krill have beneficial effects on cognition. However, the n-3 PUFA-PLs are usually a mixture of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) enriched phospholipids. Hence, the effects of EPA-PLs alone on cognitive deficiency are still unclear. In the present study, we obtained almost pure EPA-PLs (EPA:DHA = 47.9:2.08) from the sea cucumber, Cucumaria frondosa, and investigated its effects on Aβ-induced cognitive impairment in rats. Administration of EPA-PLs (150 and 300 mg/kg⋅day, i.g., 27 days) did not increase brain DHA but significantly improved Aβ-induced cognitive deficiency. Further mechanism research indicated that EPA-PLs alleviated Aβ-induced neurotoxicity including oxidative stress, apoptosis, neuro-inflammation cascade, and hyper-phosphorylated tau in a dose-dependent pattern. These findings first suggest that EPA-PLs could also improve Aβ induced cognitive deficiency in a similar mechanism with DHA-PLs.

Neurotoxicity of amyloid β (Aβ) plays an important role in Alzheimer's disease (AD) pathogenesis. In the present study, we investigated the comparative effects of docosahexaenoic acidphosphatidylcholine (DHA-PC) and docosahexaenoic acid-phosphatidylserine (DHA-PS) on Aβ-induced AD rats and studied further protective mechanisms underlying their effects. The administration of DHA-PC and DHA-PS (300 mg/kg, i.g., 27 days) had no effect on brain DHA levels but significantly improved Aβ-induced cognitive deficiency. Further mechanism research indicated that both DHA-PC and DHA-PS alleviated Aβ-induced neurotoxicity including oxidative stress, apoptosis, the neuroinflammation cascade, and hyper-phosphorylated tau. These results suggest that DHA-PC and DHA-PS represent a potential novel therapeutic candidate for the treatment of neurodegenerative diseases such as AD. Such an effect uncoupled with an increase in brain DHA but has an intimate relationship with the phospholipid polar groups, and DHA-PS has a particular advantage.

Cyclophosphamide (Cy) is the most commonly used clinical chemotherapeutic drug for cancer treatment, although it damages the microbial ecology of the gut. This study focuses on the utilisation of food-derived functional components to manipulate the gut microbiota. With a mouse model injected with Cy, the protective effect of squid ink polysaccharide (SIP) on chemotherapy-induced intestinal dysbiosis was investigated by high-throughput sequencing. The shifts in relative abundance of the dominant taxa at the phylum, class, family, and genus levels show the incredible effects of SIP. In short, SIP decreases the abundance of Ruminococcus, Bilophila, Oscillospira, Dorea and, especially, Mucispirillum, which thrives in the early disruption of the colonic surface mucus layer and induces inflammatory disorders. Our results may have important implications for the use of SIP as a functional food component with potential therapeutic utility in manipulating the gut microbiota.

The health benefits of eicosapentaenoic acid (EPA)-enriched phospholipids (PL) have witnessed a recent upsurge. In the present study, PL from starfish Asterias amurensis (SFP) and sea cucumber Cucumaria frondosa (SCP) were extracted and the liposomes were prepared. Both SFP and SCP liposomes showed antitumour effects in vitro and exhibited high transport and uptake effects in small intestinal epithelial cell models. The results also demonstrated that dietary SFP and SCP liposomes prolonged the life span and ameliorated oxidative stress status of S180 ascitic tumour-bearing mice. Results also showed that dietary SFP and SCP liposomes up-regulated the expression of Bax and down-regulated Bcl-2 level in tumour cells, then induced release of cytochrome c from mitochondria to cytosol, thus the activation of caspase 9 and caspase 3. Taken together, these findings suggest that SFP and SCP liposomes exert antitumour effects mainly via activation of mitochondrial apoptotic pathways in tumour-bearing mice. (C) 2015 Elsevier Ltd. All rights reserved.

Cancer-associated cachexia (CAC) is a multifactorial wasting syndrome which impairs quality of cancer patients' life. Cerebrosides, a principal class of sphingolipids, have various biological actions such as anti-tumour effects. In this study, we found that a continuous oral administration of cerebrosides obtained from sea cucumber Acaudina molpadioides (AMC) at 50 mg/kg body mass per day suppressed body weight loss through alleviating adipose atrophy in CAC mice. The possible mechanism by which dietary AMC prevents adipose atrophy in CAC mice was related to reducing serum inflammatory cytokine levels, regulating over-lipolysis, enhancing the function of lipogenesis and decreasing the lipid over-utilization. To elucidate the structure–activity relationships of AMC and its long-chain base (LCB), we also compared the anti-tumour activities between them. The results indicated that LCB exhibited more prominent anti-tumour effect both in vivo and in vitro. Therefore, AMC and its LCB are highly worth developing as novel agents for cancer therapy.

The amelioration in hyperglycaemia and insulin resistance of fucoidan from sea cucumber can be speculated due to these effects of fucoidan from marine phaeophyta. We examined the effect of fucoidan from Acaudina molpadioides (Am-FUC) on anti-hyperglycaemia and improvement in insulin resistance in high-fat high-sucrose diet-induced insulin resistant mice. Results showed that Am-FUC significantly reduced blood glucose, insulin, leptin, resistin, and TNF-α levels, and increased adiponectin and hepatic glycogen contents. Am-FUC improved glucose metabolism via an increase in hexokinase and pyruvate kinase activities, and a reduction in glycogen phosphorylase and glucose-6-phosphates activities. Am-FUC enhanced glucose transport through successively activated insulin signalling cascadeinduced GLUT4 translocation. Am-FUC also enhanced the effects of rosiglitazone. No signs of toxicity were observed in acute oral toxicity study. It indicates that Am-FUC acutely reduces blood glucose level and improves insulin resistance via normalization of cytokines and glucose metabolism-related enzyme activities and up-regulation of the PKB/GLUT4 pathway.

Hyperglycaemia can induce pancreatic islets apoptosis. We previously found that fucosylated chondroitin sulphate from Cucumaria frondosa (Cf-CHS) exhibited anti-hyperglycaemic effects; however, its effects on pancreatic islets are lacking. This study investigated the effects of Cf-CHS on inhibition pancreatic islets apoptosis in high-fat high-sucrose diet (HFSD)-induced insulin resistant mice for 19 weeks. Results showed that Cf-CHS significantly repaired HFSD-injured pancreatic islets, decreased blood glucose, insulin, TNF-α levels, and increased adiponectin level. Cf-CHS significantly reduced Bid, Bax, cytochrome c, caspase 9, and caspase 3 mRNA expressions, and increased Bcl-2 and Bcl-xL mRNA expressions. Cf-CHS also caused significant down-regulation of t-Bid, Bax, cytochrome c in cytoplasm, caspase 9, and cleaved-caspase 3 proteins, and up-regulation of Bcl-2 and Bcl-xL proteins. Furthermore, Cf-CHS enhanced the effects of rosiglitazone (RSG). These indicate that Cf-CHS inhibits pancreatic islets apoptosis via inhibition mitochondrial pathway. These findings may provide a dietary intervention hyperglycaemia-induced pancreatic islets apoptosis.