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Journal ArticleDOI

Prophylactic effects of sulforaphane on depression-like behavior and dendritic changes in mice after inflammation.

TLDR
Dietary intake of SFN-rich broccoli sprout could be prophylactic vegetable to prevent or minimize the relapse by inflammation in the remission state of depressed patients.
Abstract
Inflammation plays a role in the pathophysiology of depression. Sulforaphane (SFN), an isothiocyanate compound derived from broccoli, is a potent activator of the NF-E2-related factor-2 (Nrf2), which plays a role in inflammation. In this study, we examined whether the prevention effects of SFN in lipopolysaccharide (LPS) induced depression-like behavior in mice. Pretreatment with SFN significantly blocked an increase in the serum tumor necrosis factor-α (TNF-α) level and an increase in microglial activation of brain regions after a single administration of LPS (0.5 mg/kg). Furthermore, SFN significantly potentiated increased serum levels of IL-10 after LPS administration. In the tail-suspension test and forced swimming test, SFN significantly attenuated an increase of the immobility time after LPS administration. In addition, SFN significantly recovered to control levels for LPS-induced alterations in the proteins such as brain-derived neurotrophic factor, postsynaptic density protein 95 and AMPA receptor 1 (GluA1) and dendritic spine density in the brain regions. Finally, dietary intake of 0.1% glucoraphanin (a glucosinolate precursor of SFN) food during the juvenile and adolescence could prevent the onset of LPS-induced depression-like behaviors and dendritic spine changes in the brain regions at adulthood. In conclusion, these findings suggest that dietary intake of SFN-rich broccoli sprout has prophylactic effects on inflammation-related depressive symptoms. Therefore, supplementation of SFN-rich broccoli sprout could be prophylactic vegetable to prevent or minimize the relapse by inflammation in the remission state of depressed patients.

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Regulation of Gut Microbiota and Metabolic Endotoxemia with Dietary Factors.

TL;DR: The relationship between fat intake and induction of metabolic endotoxemia is summarized, focusing on gut dysbiosis and the influx, kinetics, and metabolism of LPS, and the recent findings about dietary factors that attenuate metabolic endotOxemia are summarized, focus on the regulation of gut microbiota.
Journal ArticleDOI

Blockade of interleukin-6 receptor in the periphery promotes rapid and sustained antidepressant actions: a possible role of gut–microbiota–brain axis

TL;DR: It is suggested that peripheral IL- 6 has a key role in the pathogenesis of depression and that the blockade of IL-6 receptor in the periphery might have rapid-onset and long-lasting antidepressant effects by normalizing the altered composition of gut microbiota in susceptible mice after social defeat stress.
Journal ArticleDOI

A key role of the subdiaphragmatic vagus nerve in the depression-like phenotype and abnormal composition of gut microbiota in mice after lipopolysaccharide administration.

TL;DR: The results suggest that LPS produces a depression-like phenotype, increases spleen weight, triggers inflammation, downregulates synaptic proteins in the mPFC, and leads to abnormal composition of gut microbiota via the subdiaphragmatic vagus nerve.
Journal ArticleDOI

(2R,6R)-Hydroxynorketamine is not essential for the antidepressant actions of (R)-ketamine in mice

TL;DR: Results indicate that metabolism to (2 R,6’R)-HNK is not necessary for the antidepressant effects of (R)-ketamine and that unmetabolized (R-ketamine itself may be responsible for its antidepressant actions.
References
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Journal ArticleDOI

From inflammation to sickness and depression: when the immune system subjugates the brain

TL;DR: In response to a peripheral infection, innate immune cells produce pro-inflammatory cytokines that act on the brain to cause sickness behaviour, which can lead to an exacerbation of sickness and the development of symptoms of depression in vulnerable individuals.
Journal ArticleDOI

A Meta-Analysis of Cytokines in Major Depression

TL;DR: A meta-analysis of studies measuring cytokine concentration in patients with major depression reports significantly higher concentrations of the proinflammatory cytokines TNF-alpha and IL-6 in depressed subjects compared with control subjects, strengthening evidence that depression is accompanied by activation of the IRS.
Journal ArticleDOI

Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression

TL;DR: Preliminary data from patients with inflammatory disorders, as well as medically healthy depressed patients, suggest that inhibiting proinflammatory cytokines or their signaling pathways may improve depressed mood and increase treatment response to conventional antidepressant medication.
Journal ArticleDOI

Physiology and Neurobiology of Stress and Adaptation: Central Role of the Brain

TL;DR: As an adjunct to pharmaceutical therapy, social and behavioral interventions such as regular physical activity and social support reduce the chronic stress burden and benefit brain and body health and resilience.
Journal ArticleDOI

A neurotrophic model for stress-related mood disorders.

TL;DR: Analysis of preclinical cellular and behavioral models of depression and antidepressant actions, as well as clinical neuroimaging and postmortem studies, are consistent with the hypothesis that decreased expression of BDNF and possibly other growth factors contributes to depression and that upregulation ofBDNF plays a role in the actions of antidepressant treatment.
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