TNF-α-induced depressive-like phenotype and p38MAPK activation are abolished by ascorbic acid treatment

Moretti, Morgana; Budni, Josiane; Freitas, Andiara E.; Neis, Vivian B.; Ribeiro, Camille M.; Balen, Grasiela de Oliveira; Rieger, Débora Kurrle; Leal, Rodrigo Bainy; Rodrigues, Ana Lúcia S.

doi:10.1016/j.euroneuro.2015.03.006

Cited by 45 publications

(19 citation statements)

References 49 publications

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“…Other studies have shown similar results in humans (Gautam et al 2012, Khajehnasiri et al 2013, Zhang et al 2011. Our group has demonstrated antidepressant effects of ascorbic acid in mice subjected to tail suspension test (Binfaré et al 2009), acute restraint stress (Moretti et al 2013), chronic unpredictable stress, and on the depressive-like behavior induced by administration of the pro-inflammatory cytokine tumor necrosis-alpha (Moretti et al 2012a(Moretti et al , 2012b(Moretti et al , 2015.…”

Section: Discussionsupporting

confidence: 61%

Effects of ascorbic acid on anxiety state and affect in a non-clinical sample

Moritz

Schwarzbold

Guarnieri

et al. 2017

Acta Neurobiologiae Experimentalis

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Objective Given that the literature data indicates that ascorbic acid may have an anxiolytic effect, we hypothesized that a single oral administration of ascorbic acid could acutely affect emotional states. Methods The effects of acid ascorbic supplementation on anxiety and other emotional states were evaluated by the State-Trait Anxiety Inventory (STAI), and Visual Analogue Mood Scale (VAMS). Immediately before, and 2 hours after receiving a single ascorbic acid dose (1000 mg) or placebo, 142 graduate students were evaluated by the STAI and VAMS in a randomized, double-blind, placebo-controlled trial. Results No changes from basal levels were observed in the STAI state-anxiety or VAMS scores. However, the ingestion of ascorbic acid by the 25% more anxious healthy subjects (women; 14 control and 23 ascorbic acid), as defined by the STAI trait-anxiety scale, produced a significant reduction from baseline anxiety scores in the STAI state-anxiety scale and VAMS anxiety subscale. The study evaluated a small sample with narrow sociodemographic characteristics, composed mainly of healthy young females (> 94%) enrolled in post-graduation courses, without controlling diet, physical activity, and formal psychiatric diagnosis. Conclusions: Despite the sample size limitation, this study provides the first evidence of an acute anxiolytic effect of ascorbic acid. Broader population studies are required to evaluate the clinical relevance of presented data.

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Section: Discussionsupporting

confidence: 61%

Effects of ascorbic acid on anxiety state and affect in a non-clinical sample

Moritz

Schwarzbold

Guarnieri

et al. 2017

Acta Neurobiologiae Experimentalis

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“…The JNK and ERK pathways collaboratively mediate the anti-inflammatory effects of paroxetine (Liu et al, 2014). Recent studies reported that ascorbic acid inhibits the phosphorylation of p38 MAPK in the hippocampus (Moretti et al, 2015). Regarding the effects of pro-inflammatory cytokines on the HPA axis, IL-1α inhibits GR-mediated gene transcription via p38 MAPK activation (Wang et al, 2004a).…”

Section: Effects Of Pro-inflammatory Cytokines On the Hpa Axismentioning

confidence: 99%

The role of pro-inflammatory cytokines in neuroinflammation, neurogenesis and the neuroendocrine system in major depression

Kim

Lee

Myint

et al. 2016

Progress in Neuro-Psychopharmacology and Biological Psychiatry

475

261

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Cytokines are pleiotropic molecules with important roles in inflammatory responses. Pro-inflammatory cytokines and neuroinflammation are important not only in inflammatory responses but also in neurogenesis and neuroprotection. Sustained stress and the subsequent release of pro-inflammatory cytokines lead to chronic neuroinflammation, which contributes to depression. Hippocampal glucocorticoid receptors (GRs) and the associated hypothalamus-pituitary-adrenal (HPA) axis have close interactions with pro-inflammatory cytokines and neuroinflammation. Elevated pro-inflammatory cytokine levels and GR functional resistance are among the most widely investigated factors in the pathophysiology of depression. These two major components create a vicious cycle. In brief, chronic neuroinflammation inhibits GR function, which in turn exacerbates pro-inflammatory cytokine activity and aggravates chronic neuroinflammation. On the other hand, neuroinflammation causes an imbalance between oxidative stress and the anti-oxidant system, which is also associated with depression. Although current evidence strongly suggests that cytokines and GRs have important roles in depression, they are essential components of a whole system of inflammatory and endocrine interactions, rather than playing independent parts. Despite the evidence that a dysfunctional immune and endocrine system contributes to the pathophysiology of depression, much research remains to be undertaken to clarify the cause and effect relationship between depression and neuroinflammation.

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“…Because the NOP system is widely implicated in stressrelated pathophysiology (Zhang et al, 2012b(Zhang et al, , 2015 and recent evidence suggests that cykokines can also regulate mood and psychologic responses to stress (Zhu et al, 2010;Moretti et al, 2015), a better understanding how NOP cytokine signaling, extended into nonimmune cell types, will prove critical as we attempt to understand how NOP signaling functions to bidirectionally regulate the stress response.…”

Section: Nociceptin Opioid Peptide Receptor and Inflammatory Signamentioning

confidence: 99%

Nociceptin/Orphanin FQ Receptor Structure, Signaling, Ligands, Functions, and Interactions with Opioid Systems

et al. 2016

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The NOP receptor (nociceptin/orphanin FQ opioid peptide receptor) is the most recently discovered member of the opioid receptor family and, together with its endogenous ligand, N/OFQ, make up the fourth members of the opioid receptor and opioid peptide family. Because of its more recent discovery, an understanding of the cellular and behavioral actions induced by NOP receptor activation are less well developed than for the other members of the opioid receptor family. All of these factors are important because NOP receptor activation has a clear modulatory role on mu opioid receptor-mediated actions and thereby affects opioid analgesia, tolerance development, and reward. In addition to opioid modulatory actions, NOP receptor activation has important effects on motor function and other physiologic processes. This review discusses how NOP pharmacology intersects, contrasts, and interacts with the mu opioid receptor in terms of tertiary structure and mechanism of receptor activation; location of receptors in the central nervous system; mechanisms of desensitization and downregulation; cellular actions; intracellular signal transduction pathways; and behavioral actions with respect to analgesia, tolerance, dependence, and reward. This is followed by a discussion of the agonists and antagonists that have most contributed to our current knowledge. Because NOP receptors are highly expressed in brain and spinal cord and NOP receptor activation sometimes synergizes with mu receptor-mediated actions and sometimes opposes them, an understanding of NOP receptor pharmacology in the context of these interactions with the opioid receptors will be crucial to the development of novel therapeutics that engage the NOP receptor

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TNF-α-induced depressive-like phenotype and p38MAPK activation are abolished by ascorbic acid treatment

Cited by 45 publications

References 49 publications

Effects of ascorbic acid on anxiety state and affect in a non-clinical sample

Effects of ascorbic acid on anxiety state and affect in a non-clinical sample

The role of pro-inflammatory cytokines in neuroinflammation, neurogenesis and the neuroendocrine system in major depression

Nociceptin/Orphanin FQ Receptor Structure, Signaling, Ligands, Functions, and Interactions with Opioid Systems

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