Bifidobacteria-Fermented Red Ginseng and Its Constituents Ginsenoside Rd and Protopanaxatriol Alleviate Anxiety/Depression in Mice by the Amelioration of Gut Dysbiosis

Gut dysbiosis is closely connected with the outbreak of psychiatric disorders with colitis. Bifidobacteria-fermented red ginseng (fRG) increases the absorption of ginsenoside Rd and protopanxatriol into the blood in volunteers and mice. fRG and Rd alleviates 2,4,6-trinitrobenzenesulfonic acid-induced colitis in mice. Therefore, to understand the gut microbiota-mediated mechanism of fRG against anxiety/depression, we examined the effects of red ginseng (RG), fRG, ginsenoside Rd, and protopanaxatriol on the occurrence of anxiety/depression, colitis, and gut dysbiosis in mice. Mice with anxiety/depression were prepared by being exposed to two stressors, immobilization stress (IS) or Escherichia coli (EC). Treatment with RG and fRG significantly mitigated the stress-induced anxiety/depression-like behaviors in elevated plus maze, light-dark transition, forced swimming (FST), and tail suspension tasks (TST) and reduced corticosterone levels in the blood. Their treatments also suppressed the stress-induced NF-κB activation and NF-κB+/Iba1+ cell population in the hippocampus, while the brain-derived neurotrophic factor (BDNF) expression and BDNF+/NeuN+ cell population were increased. Furthermore, treatment with RG or fRG suppressed the stress-induced colitis: they suppressed myeloperoxidase activity, NF-κB activation, and NF-κB+/CD11c+ cell population in the colon. In particular, fRG suppressed the EC-induced depression-like behaviors in FST and TST and colitis more strongly than RG. fRG treatment also significantly alleviated the EC-induced NF-κB+/Iba1+ cell population and EC-suppressed BDNF+/NeuN+ cell population in the hippocampus more strongly than RG. RG and fRG alleviated EC-induced gut dysbiosis: they increased Bacteroidetes population and decreased Proteobacteria population. Rd and protopanaxatriol also alleviated EC-induced anxiety/depression and colitis. In conclusion, fRG and its constituents Rd and protopanaxatriol mitigated anxiety/depression and colitis by regulating NF-κB-mediated BDNF expression and gut dysbiosis.

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Lacticaseibacillus paracasei NK112 mitigates Escherichia coli-induced depression and cognitive impairment in mice by regulating IL-6 expression and gut microbiota

Beneficial Microbes ◽

10.3920/bm2020.0109 ◽

2021 ◽

pp. 1-12

Author(s):

S.-W. Yun ◽

J.-K. Kim ◽

M.J. Han ◽

D.-H. Kim

Keyword(s):

Escherichia Coli ◽

Cognitive Impairment ◽

Gut Microbiota ◽

Psychiatric Disorders ◽

Myeloperoxidase Activity ◽

Bdnf Expression ◽

Strain Collection ◽

Tnf Α ◽

Faecal Bacteria ◽

Anxiety Depression

The gut microbiota communicates with the brain through microbiota-gut-brain (MGB) and hypothalamus-pituitary-adrenal (HPA) axes and other pathways. Excessive expression of interleukin (IL)-6 is closely associated with the occurrence of the psychiatric disorders depression and dementia. Therefore, to understand whether IL-6 expression-suppressing probiotics could alleviate psychiatric disorders, we isolated IL-6 expression-inhibiting Lacticaseibacillus paracasei (formerly Lactobacillus paracasei) NK112 from the human faecal bacteria strain collection (Neurobiota Research Center, Seoul, Korea) and examined its therapeutic effect for the depression and cognitive impairment in mice. C57 BL/6J mice with depression and cognitive impairment were prepared by exposure to Escherichia coli K1. Oral gavage of NK112 significantly alleviated K1-induced anxious, depressive, and memory-impaired behaviours in the elevated plus maze, tail-suspension and Y-maze tasks, IL-1β, IL-6, and tumour necrosis factor (TNF)-α expression, and nuclear factor kappa beta (NF-κB) activation in the hippocampus, while K1-suppressed brain-derived neurotrophic factor (BDNF) expression increased. Treatment with NK112 also improved K1-induced myeloperoxidase activity, IL-6 and TNF-α expression, and NF-κB activation in the colon and reduced K1-induced Proteobacteria population in the gut microbiota. Heat-killed NK112 and its lysate supernatant, and precipitate fractions also improved anxiety/depression, cognitive impairment, and colitis in mice. In conclusion, NK112, even if heat-killed or lysed, alleviated K1 stress-induced colitis, anxiety/depression, and cognitive impairment by suppressing IL-6, TNF-α, and BDNF expression through the regulation of gut microbiota and NF-κB activation.

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The Preventive and Curative Effects of Lactobacillus reuteri NK33 and Bifidobacterium adolescentis NK98 on Immobilization Stress-Induced Anxiety/Depression and Colitis in Mice

Nutrients ◽

10.3390/nu11040819 ◽

2019 ◽

Vol 11 (4) ◽

pp. 819 ◽

Cited By ~ 23

Author(s):

Hyo-Min Jang ◽

Kyung-Eon Lee ◽

Dong-Hyun Kim

Keyword(s):

Immune Responses ◽

Immobilization Stress ◽

Lactobacillus Reuteri ◽

Myeloperoxidase Activity ◽

Bdnf Expression ◽

Healthy Human ◽

Bifidobacterium Adolescentis ◽

Development Of Anxiety ◽

Anxiety Depression

The gut dysbiosis by stressors such as immobilization deteriorates psychiatric disorders through microbiota-gut-brain axis activation. To understand whether probiotics could simultaneously alleviate anxiety/depression and colitis, we examined their effects on immobilization stress (IS)-induced anxiety/depression and colitis in mice. The probiotics Lactobacillus reuteri NK33 and Bifidobacterium adolescentis NK98 were isolated from healthy human feces. Mice with anxiety/depression and colitis were prepared by IS treatment. NK33 and NK98 potently suppressed NF-κB activation in lipopolysaccharide (LPS)-induced BV-2 cells. Treatment with NK33 and/or NK98, which were orally gavaged in mice before or after IS treatment, significantly suppressed the occurrence and development of anxiety/depression, infiltration of Iba1+ and LPS+/CD11b+ cells (activated microglia) into the hippocampus, and corticosterone, IL-6, and LPS levels in the blood. Furthermore, they induced hippocampal BDNF expression while NF-κB activation was suppressed. NK33 and/or NK98 treatments suppressed IS-induced colon shortening, myeloperoxidase activity, infiltration of CD11b+/CD11c+ cells, and IL-6 expression in the colon. Their treatments also suppressed the IS-induced fecal Proteobacteria population and excessive LPS production. They also induced BDNF expression in LPS-induced SH-SY5Y cells in vitro. In conclusion, NK33 and NK98 synergistically alleviated the occurrence and development of anxiety/depression and colitis through the regulation of gut immune responses and microbiota composition.

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Buspirone alleviates anxiety, depression, and colitis; and modulates gut microbiota in mice

Scientific Reports ◽

10.1038/s41598-021-85681-w ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Jeon-Kyung Kim ◽

Sang-Kap Han ◽

Min-Kyung Joo ◽

Dong-Hyun Kim

Keyword(s):

Gut Microbiota ◽

Normal Control ◽

Cell Population ◽

Intraperitoneal Administration ◽

Fecal Microbiota ◽

Myeloperoxidase Activity ◽

Brain Functions ◽

Β Diversity ◽

Tnf Α ◽

Anxiety Depression

AbstractGut microbiota regulate the neurodevelopmental processes and brain functions through the regulation of the microbiota–gut interaction and gut–brain communication. Buspirone, an agonist for serotonin 5-HT1A receptors, is used for the treatment of anxiety/depression. Therefore, to understand the gut microbiota-mediated mechanism of buspirone on anxiety/depression, we examined its effect on the immobilization stress (IS) or Escherichia coli K1 (EC)-induced anxiety/depression in mice. Oral or intraperitoneal administration of buspirone significantly suppressed stressor-induced anxiety/depression-like behaviors in the elevated plus maze, light/dark transition, tail suspension, and forced swimming tasks. Their treatments also reduced TNF-α expression and NF-κB+/Iba1+ cell population in the hippocampus and myeloperoxidase activity and NF-κB+/CD11c+ cell population in the colon. Buspirone treatments partially restored IS- or EC-induced gut microbiota perturbation such as β-diversity to those of normal control mice: they reduced the IS- or EC-induced gut Proteobacteria population. In particular, the anxiolytic activity of buspirone was positively correlated with the populations of Bacteroides and PAC001066_g in EC- or IS-exposed mice, while the populations of Lachnospiraceae, KE159660_g, LLKB_g, Helicobacter, and PAC001228_g were negatively correlated. The anti-depressant effect of buspirone was positively correlated with the Roseburia population. The fecal microbiota transplantations from buspirone-treated mice with IS-induced anxiety/depression or normal control mice suppressed IS-induced anxiety/depression-like behaviors and reduced hippocampal NF-κB+/Iba1+ and colonic NF-κB+/CD11c+ cell populations in the transplanted mice. Furthermore, they modified IS-induced perturbation of gut microbiota composition, particularly Proteobacteria, in the transplanted mice. In conclusion, buspirone alleviates IS as well as EC-induced anxiety/depression and colitis. It also suppresses associated neuroinflammation and modulates gut microbiota. Future studies can help to explain the relationship, if any, in the central and peripheral effects of buspirone.

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Chaihu-Shugan-San (Shihosogansan) alleviates restraint stress-generated anxiety and depression in mice by regulating NF-κB-mediated BDNF expression through the modulation of gut microbiota

Chinese Medicine ◽

10.1186/s13020-021-00492-5 ◽

2021 ◽

Vol 16 (1) ◽

Author(s):

Sang-Kap Han ◽

Jeon-Kyung Kim ◽

Hee-Seo Park ◽

Yeun-Jeong Shin ◽

Dong-Hyun Kim

Keyword(s):

Gut Microbiota ◽

Restraint Stress ◽

Corticosterone Level ◽

Anxiety And Depression ◽

Enzyme Linked Immunosorbent Assay ◽

Myeloperoxidase Activity ◽

Bdnf Expression ◽

Fecal Transplantation ◽

Gut Dysbiosis ◽

Freeze Dried

Abstract Background Chaihu-Shugan-San (CSS, named Shihosogansan in Korean), a Chinese traditional medicine, is frequently used to treat anxiety and depression. Psychiatric disorders including depression are associated with gut dysbiosis. Therefore, to comprehend gut microbiota-involved anti-depressive effect of CSS, we examined its effect on restraint stress (RS)-induced depression and gut dysbiosis in mice Methods CSS was extracted with water in boiling water bath and freeze-dried. Anxiety and depression was induced in C57BL/6 mice by exposure to RS. Anxiety- and depression-like behaviors were measured in the light/dark transition and elevated plus maze tasks, forced swimming test, and tail suspension test. Biomarkers were assayed by using the enzyme-linked immunosorbent assay and immunoblotting. The gut microbiota composition was analyzed by Illumina iSeq sequencer. Results CSS significantly reduced the RS-induced anxiety- and depression-like behaviors in mice. CSS suppressed the RS-induced activation of NF-κB and expression of interleukin (IL)-6 and increased the RS-suppressed expression of brain-derived neurotrophic factor (BDNF). Furthermore, CSS suppressed the RS-induced IL-6 and corticosterone level in the blood and IL-6 expression and myeloperoxidase activity in the colon. CSS decreased the RS-induced γ-Proteobacteria population in gut microbiota, while the RS-suppressed Lactobacillaceae, Prevotellaceae, and AC160630_f populations increased. Fecal transplantation of vehicle-treated control or RS/CSS-treated mice into RS-exposed mice significantly mitigated RS-induced anxity- and depression-like behaviors, suppressed the NF-κB activation in the hippocampus and colon, and reduced the IL-6 and corticosterone levels in the blood. These fecal microbiota transplantations suppressed RS-induced Desulfovibrionaceae and γ-Proteobacteria populations and increased RS-suppressed Lactobacillaceae and Prevotellaceae poulation in the gut microbiota. Conclusions CSS alleviated anxiety and depression by inducing NF-κB-involved BDNF expression through the regulation of gut inflammation and microbiota.

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Transplantation of fecal microbiota from patients with inflammatory bowel disease and depression alters immune response and behavior in recipient mice

Scientific Reports ◽

10.1038/s41598-021-00088-x ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Hyo-Min Jang ◽

Jeon-Kyung Kim ◽

Min-Kyung Joo ◽

Yoon-Jung Shin ◽

Chang Kyun Lee ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Gut Microbiota ◽

Cell Population ◽

Bowel Disease ◽

Fecal Microbiota ◽

Cell Populations ◽

Microbiota Composition ◽

Gut Dysbiosis ◽

Inflammatory Bowel ◽

Anxiety Depression

AbstractGut dysbiosis is closely associated with the occurrence of inflammatory bowel disease (IBD) and psychiatric disorder. Here, to understand the difference of gut microbiota composition and physiological effect between IBD patients with (IBD/D+) or without depression (IBD/D−), we analyzed the fecal microbiota composition of patients with IBD with (/D+) or without depression (/D−) and healthy volunteers (HVs) and examined the effects of these fecal microbiota transplantations (FMTs) on the occurrence of systemic inflammation and anxiety/depression in mice. FMTs from patients with IBD/D+ or IBD/D− caused IBD-like colitis in the transplanted mice: they increased the myeloperoxidase activity, IL-1β and IL-6 expression, and NF-κB+/CD11c+ cell population in the colon. Transplantation of the IBD/D+ patient feces (IBD/D+-F) caused IBD-like colitis more strongly than that of IBD/D−-F. FMTs from patients with IBD/D+ also caused anxiety-/depression-like behaviors, increased the NF-κB+/Iba1+ and lipopolysaccharide (LPS)+/Iba1+ cell populations, and decreased the BDNF+/NeuN+ cell population in the hippocampus. They increased LPS levels in the blood. FMTs from patients with IBD/D− caused anxiety-like, but not depression-like, behaviors. α-/β-diversities and composition of gut microbiota in IBD-F were different from those of HV feces (HV-F). The Enterobacteriaceae and Enterococcaceae populations and LPS levels were higher in the IBD-F than in the HV-F. The Enterococcaceae population was higher in IBD/D+-F vs. IBD/D−-F. However, the transplantation of HV-F into mice previously transplanted with IBD/D+-F significantly reduced depression-like behaviors, NF-κB+/Iba1+ and LPS+/Iba1+ cell populations in the hippocampus, LPS levels in the feces and blood, and IL-1β expression in the colon. These findings suggest that the outbreak of depression/anxiety may be dependent on the systemic inflammation with a leaky gut through the gut dysbiosis-attributable overproduction of bacterial LPS and suppression of tight junction protein expression in patients with IBD.

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Grewia asiatica Berry Juice Diminishes Anxiety, Depression, and Scopolamine-Induced Learning and Memory Impairment in Behavioral Experimental Animal Models

Frontiers in Nutrition ◽

10.3389/fnut.2020.587367 ◽

2021 ◽

Vol 7 ◽

Author(s):

Imran Imran ◽

Sana Javaid ◽

Aroosa Waheed ◽

Muhammad Fawad Rasool ◽

Abdul Majeed ◽

...

Keyword(s):

Learning And Memory ◽

Forced Swim Test ◽

Behavioral Assessment ◽

Central Zone ◽

Experimental Models ◽

Object Recognition Test ◽

Y Maze ◽

Plus Maze ◽

Anxiety Depression ◽

The Brain

Grewia asiatica L. fruit natively called phalsa is a popular berry of Pakistan and widely consumed in the form of fresh juices and carbonated drinks in the summer season. The berry is enriched with antioxidants such as phenols, flavonoids, anthocyanins, and vitamin C. Scientifically, it is the least explored berry in terms of neuromodulatory activities, and therefore, in the designed study, chronically fed rats with the different dilutions (5%−30%) of fruit juice were subjected to behavioral assessment for anxiety, depression, and cognition (spatial memory) followed by biochemical analysis of isolated brains. Results revealed a prominent impact of 20 and 30% dilutions of fruit exudate as treated animals showed anxiolytic behavior to central zone (P < 0.05) of open field test (OFT) and open arms of elevated plus maze (EPM) (P < 0.05) in anxiety models. Overall, immobility of rats treated with a higher concentration of exudate in forced swim test (FST) was reduced (P < 0.05) presenting antidepressant-like activity. Moreover, in learning and memory experimental models, the treated animals reversed scopolamine-induced amnesic effects as evident from improved step-through latencies (P < 0.05 vs. scopolamine; passive avoidance test), spontaneous alternation behavior (P < 0.05 vs. scopolamine; Y-maze test), discrimination index (P < 0.05 vs. scopolamine; novel object recognition test), and escape latencies (P < 0.05 vs. scopolamine; Morris water maze). Biochemical studies of isolated brains from treated rats demonstrated significantly elevated levels of superoxide dismutase and glutathione peroxidase (P < 0.05), whereas levels of acetylcholinesterase and malondialdehyde level (P < 0.05) were reduced, indicating its potential to reduce oxidative damage in the brain and modulation with the cholinergic system. The outcomes of studies support the benefits of phytoconstituents possessed by G. asiatica fruit in the amelioration of neurological disorders that could be due to their antioxidative capacity or due to interaction with GABAergic, serotonergic, and cholinergic systems in the brain.

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Gut Microbiota and Dysbiosis in Alzheimer’s Disease: Implications for Pathogenesis and Treatment

Molecular Neurobiology ◽

10.1007/s12035-020-02073-3 ◽

2020 ◽

Vol 57 (12) ◽

pp. 5026-5043 ◽

Cited By ~ 2

Author(s):

Shan Liu ◽

Jiguo Gao ◽

Mingqin Zhu ◽

Kangding Liu ◽

Hong-Liang Zhang

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Gut Microbiota ◽

Gut Dysbiosis ◽

Bidirectional Communication ◽

Significant Research ◽

Novel Therapeutic Strategies ◽

The Brain ◽

Brain Homeostasis ◽

Gut Microbiota Composition

Abstract Understanding how gut flora influences gut-brain communications has been the subject of significant research over the past decade. The broadening of the term “microbiota-gut-brain axis” from “gut-brain axis” underscores a bidirectional communication system between the gut and the brain. The microbiota-gut-brain axis involves metabolic, endocrine, neural, and immune pathways which are crucial for the maintenance of brain homeostasis. Alterations in the composition of gut microbiota are associated with multiple neuropsychiatric disorders. Although a causal relationship between gut dysbiosis and neural dysfunction remains elusive, emerging evidence indicates that gut dysbiosis may promote amyloid-beta aggregation, neuroinflammation, oxidative stress, and insulin resistance in the pathogenesis of Alzheimer’s disease (AD). Illustration of the mechanisms underlying the regulation by gut microbiota may pave the way for developing novel therapeutic strategies for AD. In this narrative review, we provide an overview of gut microbiota and their dysregulation in the pathogenesis of AD. Novel insights into the modification of gut microbiota composition as a preventive or therapeutic approach for AD are highlighted.

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BDNF and nicotine dependence: associations and potential mechanisms

Reviews in the Neurosciences ◽

10.1515/revneuro-2020-0044 ◽

2020 ◽

Vol 0 (0) ◽

Author(s):

Zeyi Huang ◽

Daichao Wu ◽

Xilin Qu ◽

Meixiang Li ◽

Ju Zou ◽

...

Keyword(s):

Nicotine Dependence ◽

Nicotinic Acetylcholine Receptors ◽

Acetylcholine Receptors ◽

Molecular Mechanisms ◽

Public Health Problem ◽

Nicotine Addiction ◽

Tyrosine Kinase Receptor ◽

Bdnf Expression ◽

High Affinity Receptor ◽

The Brain

AbstractSmoking is the leading preventable cause of death worldwide and tobacco addiction has become a serious public health problem. Nicotine is the main addictive component of tobacco, and the majority of people that smoke regularly develop nicotine dependence. Nicotine addiction is deemed to be a chronic mental disorder. Although it is well known that nicotine binds to the nicotinic acetylcholine receptors (nAChRs) and activates the mesolimbic dopaminergic system (MDS) to generate the pleasant and rewarding effects, the molecular mechanisms of nicotine addiction are not fully understood. Brain-derived neurotrophic factor (BDNF) is the most prevalent growth factor in the brain, which regulates neuron survival, differentiation, and synaptic plasticity, mainly through binding to the high affinity receptor tyrosine kinase receptor B (TrkB). BDNF gene polymorphisms are associated with nicotine dependence and blood BDNF levels are altered in smokers. In this review, we discussed the effects of nicotine on BDNF expression in the brain and summarized the underlying signaling pathways, which further indicated BDNF as a key regulator in nicotine dependence. Further studies that aim to understand the neurobiological mechanism of BDNF in nicotine addcition would provide a valuable reference for quitting smoking and developing the treatment of other addictive substances.

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Low frequency deep brain stimulation in the inferior colliculus ameliorates haloperidol-induced catalepsy and reduces anxiety in rats

PLoS ONE ◽

10.1371/journal.pone.0243438 ◽

2020 ◽

Vol 15 (12) ◽

pp. e0243438

Author(s):

Hannah Ihme ◽

Rainer K. W. Schwarting ◽

Liana Melo-Thomas

Keyword(s):

Deep Brain Stimulation ◽

Brain Stimulation ◽

Low Frequency ◽

Anxiolytic Effect ◽

Motor Deficits ◽

Sham Treatment ◽

Plus Maze ◽

Aversive Behavior ◽

The Brain ◽

Deep Brain

Deep brain stimulation (DBS) of the colliculus inferior (IC) improves haloperidol-induced catalepsy and induces paradoxal kinesia in rats. Since the IC is part of the brain aversive system, DBS of this structure has long been related to aversive behavior in rats limiting its clinical use. This study aimed to improve intracollicular DBS parameters in order to avoid anxiogenic side effects while preserving motor improvements in rats. Catalepsy was induced by systemic haloperidol (0.5mg/kg) and after 60 min the bar test was performed during which a given rat received continuous (5 min, with or without pre-stimulation) or intermittent (5 x 1 min) DBS (30Hz, 200–600μA, pulse width 100μs). Only continuous DBS with pre-stimulation reduced catalepsy time. The rats were also submitted to the elevated plus maze (EPM) test and received either continuous stimulation with or without pre-stimulation, or sham treatment. Only rats receiving continuous DBS with pre-stimulation increased the time spent and the number of entries into the open arms of the EPM suggesting an anxiolytic effect. The present intracollicular DBS parameters induced motor improvements without any evidence of aversive behavior, pointing to the IC as an alternative DBS target to induce paradoxical kinesia improving motor deficits in parkinsonian patients.

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DHA/EPA SUPPLEMENTATION DECREASES ANXIETY-LIKE BEHAVIOUR, BUT IT DOES NOT AMELIORATE METABOLIC PROFILE IN OBESE MALE RATS

British Journal Of Nutrition ◽

10.1017/s0007114521003998 ◽

2021 ◽

pp. 1-25

Author(s):

João Neto ◽

Jeferson Jantsch ◽

Simone de Oliveira ◽

Matheus Filipe Braga ◽

Luís Felipe dos Santos de Castro ◽

...

Keyword(s):

Public Health Problem ◽

Male Rats ◽

Major Public Health Problem ◽

Omega 3 ◽

Elevated Plus Maze Test ◽

Tnf Α ◽

Plus Maze ◽

Neuropsychiatric Diseases ◽

The Brain ◽

Diet Model

Abstract Obesity is a major public health problem that predisposes to several diseases and higher mortality in patients with COVID-19. Obesity also generates neuroinflammation, which predisposes to the development of neuropsychiatric diseases. Since there is a lack of effective treatments for obesity, the search for new strategies to reverse its consequences is urgent. In this perspective, the anti-inflammatory properties of omega-3 polyunsaturated fatty acids such as DHA/EPA might reduce the harmful effects of obesity. Here, we used the cafeteria diet model to induce obesity in Wistar rats. Animals received ultra-processed food for 20 weeks, and DHA/EPA supplementation (500mg/Kg/day) was performed between the 16th and the 20th week. At the end of the experiment, it was evaluated: body weight, visceral fat deposition, plasma glucose, insulin and triglycerides, and it was also measured the levels of inflammatory cytokines TNF-α and IL-6 in plasma and liver, and TNF-α in the prefrontal cortex. The elevated plus-maze test was performed to analyze anxiety-like behaviour. Our results demonstrated that DHA/EPA could not reverse weight and fat gain and did not modify plasma dosages. However, there was a decrease in IL-6 in the liver (DHA/EPA effect: p = 0.023) and TNF-α in the brain (CAF compared to CAF+DHA/EPA, p < 0.05). Also, there was a decrease in the anxiety index in CAF+DHA/EPA compared to the CAF group (p < 0.01). Thus, DHA/EPA supplementation is helpful to reverse the consequences of obesity in the brain.

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