PMID: 

Food Funct. 2020 Mar 31. Epub 2020 Mar 31. PMID: 32232254

Abstract Title: 

Astaxanthin (ATX) enhances the intestinal mucosal functions in immunodeficient mice.

Abstract: 

Increasing pressure of life may bring some disease risks and stress injuries, which may destroy the immune system and result in intestinal mucosal immune disorders. In this study, the effects of different doses of ATX (30 mg per kg b.w., 60 mg per kg b.w. and 120 mg per kg b.w.) on intestinal mucosal functions were explored in cyclophosphamide (Cy)-induced immunodeficient mice. The results showed that continuous intraperitoneal injection of 100 mg per kg b.w. Cy for three days led to a persistent decrease of body weight and a range of abnormalities in the intestine of C57BL/6 mice. However, administration of ATX at 60 and 120 mg per kg b.w. could effectively prevent intestinal mucosa from this damage, including reduced levels of oxidative stress (MDA, GSH and GSH-PX), increased intestinal morphological structural integrity, stimulative growth of goblet cells and mucous secretion, decreased development of Paneth cells and expression levels of antimicrobial peptides (AMPs) (Reg-3γ and lysozyme), increased IgA secretion, ameliorative main gut flora (especially total bacteria, Lactobacillus and Enterobacteriaceae spp. ) and its metabolites (acetic acid, propionic acid and butyric acid). These protective effects of ATX were better than those of control-β-carotene in general.Our results may provide a new protective measure to keep intestinal mucosal barriers, which is of great significance for maintaining immune function in the body.

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PMID: 

Naunyn Schmiedebergs Arch Pharmacol. 2020 Apr 11. Epub 2020 Apr 11. PMID: 32279084

Abstract Title: 

Astaxanthin alleviates gestational diabetes mellitus in mice through suppression of oxidative stress.

Abstract: 

Gestational diabetes mellitus (GDM) affects 7% of pregnant women worldwide, which increases the risk of diabetes and cardiovascular disease for both the mother and the fetus. Natural compound Astaxanthin has been reported to have benefits in obesity and diabetes. A pregnant C57BL/KsJ db/+ mouse was used as a genetic GDM model to investigate the effect of Astaxanthin on GDM symptoms and reproductive outcomes. Blood glucose, plasma insulin, glucose intolerance, insulin sensitivity, biochemical indexes of plasma, and the liver were measured; Nrf2 and HO-1 protein levels were detected by Western blotting. Astaxanthin significantly alleviated the glucose intolerance andβ cell insufficiency, inhibited in vivo oxidative stress, enhanced the activity of antioxidant enzymes, and improved reproductive outcomes. Mechanistically, the effect of Astaxanthin was mediated by restoring the Nrf2/HO-1 antioxidant pathway in the liver of GDM mice. Our findings supported that Astaxanthin was a potential therapeutic reagent for not only diabetes but also GDM symptomology.

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PMID: 

Neurosci Res. 2020 Apr 22. Epub 2020 Apr 22. PMID: 32333925

Abstract Title: 

Astaxanthin suppresses endoplasmic reticulum stress and protects against neuron damage in Parkinson's disease by regulating miR-7/SNCA axis.

Abstract: 

Parkinson's disease (PD) is a common neurodegenerative disorder that featured by the loss of dopaminergic neurons. Astaxanthin (AST), an important antioxidant, is demonstrated to be a neuroprotective agent for PD. However, the underlying mechanisms of AST in PD remain largely unclear. In this study, we found that AST treatment significantly not only abolished the cell viability inhibition and apoptosis promotion induced by 1-methyl-4-phenylpyridinium (MPP+) in SH-SY5Y cells via inhibiting endoplasmic reticulum (ER) stress, but also reversed the MPP + caused dysregulation of miR-7 and SNCA expression. MiR-7 knockdown and SNCA overexpression were achieved by treating SH-SY5Y cells with miR-7 inhibitor and pcDNA3.1-SNCA plasmids, respectively. MiR-7 could bind to and negatively regulate SNCA in SH-SY5Y cells. Treated SH-SY5Y cells with miR-7inhibitor or pcDNA3.1-SNCA abrogated the protective effects of AST on MPP + induced cytotoxicity. Knockdown of miR-7 aggravated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced neuron injury in vivo suggested by athletic performance, histopathological morphology, expression of tyrosine hydroxylase (TH) and TUNEL positvie cells, however, AST treatment could reverse these effects of miR-7 knockdown. Collectively, AST suppressed ER stress and protected against PD-caused neuron damage by targeting miR-7/SNCA axis, implying that AST might be a potential effective therapeutic agent for PD.

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PMID: 

Food Funct. 2020 Apr 28. Epub 2020 Apr 28. PMID: 32343758

Abstract Title: 

Astaxanthin attenuates d-galactose-induced brain aging in rats by ameliorating oxidative stress, mitochondrial dysfunction, and regulating metabolic markers.

Abstract: 

Astaxanthin (AX) is a red-colored xanthophyll carotenoid with potent antioxidant, anti-inflammatory, and neuroprotective properties. However, the underlying in vivo mechanism by which AX protects the brain from oxidative stress remains unclear. In this study, we investigated the protective effect of AX on brain oxidative damage in a d-galactose-induced rat model of aging. We also explored its possible mechanism of action by analyzing the resulting serum metabolic profiles. Our results showed that AX significantly increased the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) by 26%, 30%, and 53%, respectively. AX also significantly increased the mitochondrial membrane potential by 18% when compared with the model group. Additionally, treatment with AX (15 mg kg-1) increased the activities of respiratory chain complexes I and IV by 50.17% and 122.87%, respectively. Furthermore, AX also improved age-related morphological changes in the cerebral cortex and hippocampus. Significant differences in serum metabolic profiles were observed between the d-galactose and AX treatment groups. AX corrected amino acid metabolic problems by increasing the levels of N-acetyl-l-leucine, N-acetyl-l-tyrosine, and methionine sulfoxide to protect nerve cells. This also allowed AX to regulate the pentose phosphate pathway by acting on ergotoxine, d-xylose-5-phosphoric, and thiamine, to against oxidative stress and apoptosis. Moreover, AX reduced the levels of both hyodeoxycholic acid and chenodeoxycholic acid though the primary bile acid biosynthesis pathway, resulting in improved brain mitochondrial dysfunction. In conclusion, AX likely enhances the brain's antioxidant defenses through these potential metabolic means, enabling the brain to resist mitochondrial dysfunction, improve neuronal damage, and protect the electron transmission of mitochondrial respiratory chain, thus preventing brain aging.

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PMID: 

Cell J. 2021 Jan ;22(4):565-571. Epub 2020 Apr 22. PMID: 32347051

Abstract Title: 

Astaxanthin Reduces Demyelination and Oligodendrocytes Death in A Rat Model of Multiple Sclerosis.

Abstract: 

Objective: Astaxanthin (AST) is a carotenoid with anti-oxidative, anti-inflammatory, and anti-apoptotic properties. It has also been reported that AST exerts protective effects against neurodegenerative diseases and reduces oxidative stress-induced the central nervous system (CNS) injury. In this study, we aimed to evaluate the protective potential of AST in inhibiting demyelination and oligodendrocyte death in a rat model of multiple sclerosis (MS).Materials and Methods: In this experimental study, forty Wistar rats were randomly assigned to four experimental groups: control group (with normal feeding), cuprizone (CPZ group) that daily received 0.6% CPZ for 4 weeks, sham group that daily received 0.6% CPZ plus dimethyl sulfoxid (DMSO) for 4 weeks, and AST group that daily received 0.6% CPZ and after 12 hours were treated with AST (3 mg/kg), for 4 weeks. Muscle strength was evaluated by the behavioral basket test at the end of every week for 4 weeks. Luxol Fast Blue (LFB) staining was utilized for the identification of myelination and demyelination. Myelin density was evaluated by the ImageJ software. The expression of A2B5 (oligodendrocyte precursor protein) and myelin oligodendrocyte protein (MOG) were assessed by immunohistochemistry (IHC) and the expression of myelin basic protein, MOG, and platelet-derived growth factor-alphagenes was examined by the real-time polymerase chain reaction (RT-PCR) technique.Results: The administration of AST reduced the oligodendrocyte damage and myelin sheath disruption in a rat model of MS. The basket behavioral test showed the improvement of muscle strength in the AST group compared with CPZ and sham groups. Besides, the results of real-time PCR and IHC indicated the beneficial effects of AST in declining demyelination and oligodendrocyte death in a rat model of MS.Conclusion: AST reduces damages to the myelin sheath and oligodendrocyte death in a rat model of MS.

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PMID: 

Prostaglandins Leukot Essent Fatty Acids. 2020 Apr ;155:102077. Epub 2020 Feb 21. PMID: 32145667

Abstract Title: 

Concentrates of buttermilk and krill oil improve cognition in aged rats.

Abstract: 

Cognitive decline is one of the hallmarks of aging and can vary from mild cognitive impairment to dementia to Alzheimer's disease. In addition to some lifestyle interventions, there is room for the use of nutraceuticals/functional foods as pharma-nutritional tools to lessen the burden of cognitive decline before it worsens. We previously reported the promising molecular actions of milk fat globule membranes and krill oil concentrates in a rat model of aging. In this study, we concentrated on the activities on cognition, using an array of validated tests. We also performed lipidomic analyses of plasma, erythrocytes, and different brain areas. We report lower emotional memory (contextual fear conditioning) in aged rats supplemented with concentrates of polar lipids from buttermilk or krill oil at doses that approximate human consumption. No other behavioral parameter was significantly influenced by the supplements, calling for further research to confirm or not the purported salubrious activities of polar lipids, namely those rich inω3 long-chain polyunsaturated fatty acids, on cognitive decline.

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PMID: 

Int J Nanomedicine. 2019 ;14:8305-8320. Epub 2019 Nov 6. PMID: 31806959

Abstract Title: 

Krill Oil-Incorporated Liposomes As An Effective Nanovehicle To Ameliorate The Inflammatory Responses Of DSS-Induced Colitis.

Abstract: 

Background: Phosphatidylcholine (PC) and Omega-3 fatty acid (Omega-3) are promising therapeutic molecules for treating inflammatory bowel disease (IBD).Purpose: Based on the IBD therapeutic potential of nanoparticles, we herein sought to develop Omega-3-incorporated PC nanoparticles (liposomes) as an orally administrable vehicle for treating IBD.Methods: Liposomes prepared with or without Omega-3 incorporation were compared in terms of colloidal stability and anitiinflammatory effects.Results: The incorporation of free Omega-3 (alpha-linolenic acid, eicosapentaenoic acid or docosahexaenoic acid) into liposomes induced time-dependent membrane fusion, resulting in particle size increase from nm toμm during storage. In contrast, krill oil incorporation into liposomes (KO liposomes) did not induce the fusion and the particle size maintained

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PMID: 

Brain Behav Immun. 2020 Jan 24. Epub 2020 Jan 24. PMID: 31987923

Abstract Title: 

Depressive-like phenotype evoked by lifelong nutritional omega-3 deficiency in female rats: Crosstalk among kynurenine, Toll-like receptors and amyloid beta oligomers.

Abstract: 

Depression is one of the most common psychiatric diseases and the prevalence of depressive symptoms in women is almost twice compared to men, although the reasons of this gender difference are not fully understood yet. Recently, soluble amyloid beta (Aβ)peptide has been receiving great importance in the development of depression, also considering that depression is highly comorbid with Alzheimer's disease and other neurodegenerative illnesses. The central role played by Aβ in the development of depressive-like symptoms in rodents has been evidenced in environmental rodent model of depression. Indeed, we have previously found that lifelong exposure to n-3 polyunsaturated fatty acids (PUFA) deficient diet in female rats at 8 weeks of life leads to depressive like- symptoms and higher susceptibility to stress associated with increased Aβ levels. In order to understand if such effects were maintained over time, rats were exposed to the same diet regimen until 6 or 21 weeks of life. We found that both timepoints of exposure to n-3 PUFA deficient diet lead to depressive-like phenotype. Furthermore, a significant alteration in brain neurochemistry was retrieved. In particular, in hippocampal area a significant reduction in serotonin (5-HT) and noradrenaline (NA) content was evidenced. Considering the prominent role of NA in counterbalancing neuroinflammatory state, we quantified in the same brain area kynurenine levels, a metabolite of tryptophan implicated in inflammatory state and brought to the fore for its implication in depression. Interestingly, kynurenine levels were significantly increased in hippocampus (HIPP) of female rats exposed to such diet. In addition, lifelong deficiency in n-3 PUFA dietary intake led to systemic increase of corticosterone, hence hypothalamic pituitary adrenal (HPA) axis hyperactivation, and higher proinflammatory cytokine production. Increased production of kynurenine, along with HPA axis hyperactivation, havebeen associated with immune system modulation, particularly through Toll-like receptor type 2 (TLR2) and Toll-like receptor type 4 (TLR4) involvement. In addition, it has been shown that soluble forms of Aβcan induced depressive like-phenotype in consequence to a crosstalk between TLR4 and 5-HTergic system. Thus, considering that in this model we have previously reported increased plasma Aβlevel, we quantified TRL2 and 4 expression in HIPP of treated rats. We found that chronic exposure to a diet characterized by very low n-3 PUFA content led to higher expression of TLR2 and TLR4 in HIPP of female treated rats, indicating an activation of the immune system and was accompanied by increased expression of oligomeric Aβ. Taken together, our data indicate that the pro-depressive effects induced by a diet poor in n-3 PUFA can be attributable to a shift of hippocampal tryptophan metabolism toward inflammatory metabolite ultimately corresponding to altered immune response and increased Aβ oligomerization.

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PMID: 

J Interferon Cytokine Res. 2020 Mar 13. Epub 2020 Mar 13. PMID: 32176565

Abstract Title: 

Omega 3 Supplementation Can Regulate Inflammatory States in Gas Station Workers: A Double-Blind Placebo-Controlled Clinical Trial.

Abstract: 

Environmental exposure to diesel particulate matter and commercial gasoline in gas station workers might induce oxidative stress and changes in the balance of the immune system. In this study, the immunomodulatory impacts of omega 3 fatty acid (ω3FA) supplement were assessed on inflammatory and anti-inflammatory markers in gas station workers in a double-blind placebo-controlled clinical trial. Fifty-three men working in gas stations were treated with ω3FA ( = 29) or placebo ( = 24) for 60 days. C-reactive protein, interleukin-12 (IL-12), transforming growth factor β (TGF-β), interferon γ (IFN-γ), tumor necrosis factor α, IL-10, and IL-17 levels were measured by enzyme-linked immunosorbent assay method before and after the completion of the trial. The concentrations of IFN-γ and IL-17 were significantly decreased in ω3FA group compared with the placebo group ( 

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PMID: 

Nutrients. 2020 Apr 23 ;12(4). Epub 2020 Apr 23. PMID: 32340216

Abstract Title: 

Optimal Nutritional Status for a Well-Functioning Immune System Is an Important Factor to Protect against Viral Infections.

Abstract: 

Public health practices including handwashing and vaccinations help reduce the spread and impact of infections. Nevertheless, the global burden of infection is high, and additional measures are necessary. Acute respiratory tract infections, for example, were responsible for approximately 2.38 million deaths worldwide in 2016. The role nutrition plays in supporting the immune system is well-established. A wealth of mechanistic and clinical data show that vitamins, including vitamins A, B, B, C, D, E, and folate; trace elements, including zinc, iron, selenium, magnesium, and copper; and the omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid play important and complementary roles in supporting the immune system. Inadequate intake and status of these nutrients are widespread, leading to a decrease in resistance to infections and as a consequence an increase in disease burden. Against this background the following conclusions are made: (1) supplementation with the above micronutrients and omega-3 fatty acids is a safe, effective, and low-cost strategy to help support optimal immune function; (2) supplementation above the Recommended Dietary Allowance (RDA), but within recommended upper safety limits, for specific nutrients such as vitamins C and D is warranted; and (3) public health officials are encouraged to include nutritional strategies in their recommendations to improve public health.

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