Effects of the total flavonoid extract of Xiaobuxin-Tang on depression-like behavior induced by lipopolysaccharide and proinflammatory cytokine levels in mice

Liu, An; Li, Jing; Yu, Songtao; Xue, Rui; Yu, Na; Chen, Hongxia; Zhang, Liming; Zhao, Nan; Li, Yunfeng; You-zhi, Zhang

doi:10.1016/j.jep.2015.01.022

Cited by 22 publications

(12 citation statements)

References 35 publications

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“…In general, minocycline and cytokine antagonists are effective to block inflammation-induced depression when administered before immune stimulation. The same effect is obtained with a wide variety of anti-inflammatory or anti-oxidant natural compounds, such as curcumin, apigenine, honkiol, xiaobuxin-tang flavonoid extract, perillaldehyde, ginseng saponins, and alpha-tocopherol (Wang et al 2014; Li et al 2015a; Sulakhiya et al 2014; An et al 2015; Ji et al 2014; Kang et al 2011; Manosso et al 2013). However, it is not known whether the anti-inflammatory treatment can block behavioral signs of depression once they have developed.…”

Section: Targeting Inflammation-induced Depression: Translational Aspmentioning

confidence: 70%

Role of the Kynurenine Metabolism Pathway in Inflammation-Induced Depression: Preclinical Approaches

Dantzer

2016

Current Topics in Behavioral Neurosciences

201

151

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Physically ill patients with chronic inflammation often present with symptoms of depression. Our understanding of the pathophysiology of inflammation-associated depression has benefited from preclinical studies on the mechanisms of sickness and clinical studies on the symptoms of sickness and depression that develop in patients treated with immunotherapy. Sickness behavior develops when the immune system is activated by pathogen- or damage-associated molecular patterns. It is a normal biological response to infection and cell injury. It helps the organism to mobilize its immune and metabolic defenses to fight the danger. Depression emerges on the background of sickness when the inflammatory response is too intense and long lasting or the resolution process is deficient. The transition from sickness to depression is mediated by activation of the kynurenine metabolism pathway that leads to the formation of neurotoxic kynurenine metabolites including quinolinic acid, an agonist of N-methyl-D-aspartate receptors. The neuroimmune processes and molecular factors that have been identified in the studies of inflammation-associated depression represent potential new targets for the development of innovative therapies for the treatment of major depressive disorders.

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Section: Targeting Inflammation-induced Depression: Translational Aspmentioning

confidence: 70%

Role of the Kynurenine Metabolism Pathway in Inflammation-Induced Depression: Preclinical Approaches

Dantzer

2016

Current Topics in Behavioral Neurosciences

201

151

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“…One hour after oral administration (the same as for the TST and FST procedures), the locomotor activity was estimated as previously described (An et al, ). The numbers of crossings and rearings in 5 min were recorded.…”

Section: Methodsmentioning

confidence: 99%

Inulin‐Type Oligosaccharides Extracted from Yacon Produce Antidepressant‐Like Effects in Behavioral Models of Depression

Liu

Yang²,

Yin

et al. 2016

Phytotherapy Research

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Yacon (Smallanthus sonchifolius), a traditional food in the Andean diet, is attracting global attention for its medicinal properties, which are mainly because of its high content of non-digestible oligosaccharides. The purpose of this study is to evaluate the antidepressant-like effects of inulin-type oligosaccharides extracted from yacon (YOs) in behavioral models of depression. Behavioral despair models in mice including the tail suspension test (TST) and the forced swimming test (FST) were used to determine the effects of acute YOs administration. The locomotor activity was also explored to eliminate any false-positive activity. In addition, to further investigate the antidepressant-like effects of subchronic YOs administration, the learned helplessness (LH) paradigm in rats was performed. The results demonstrated that YOs (25, 50, or 100 mg/kg, p.o.) treatment significantly reduced the immobility time in the mouse TST and FST in a U-shaped, dose-dependent manner, and showed no stimulatory effect on the locomotor activity. Furthermore, subchronic YOs (25, 50, or 100 mg/kg, p.o.) treatment significantly reversed the escape deficits in LH rats, including an increased number of escape failures and prolonged escape latency. These findings suggest that the inulin-type oligosaccharides extracted from yacon may be a prospective natural source for antidepressants. Copyright © 2016 John Wiley & Sons, Ltd.

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“…Interferon-gamma is a crucial component in this model, as transgenic animals with deletion of its receptor do not show depressive-like behaviors ( O’Connor et al, 2009b ). Likewise, many laboratories have continued to demonstrate that a variety of antiinflammatory compounds abrogate or attenuate depressive-like behaviors using this model ( Ferreira Mello et al, 2013 ; Ji et al, 2014 ; Ma et al, 2014 ; Wang et al, 2014 ; An et al, 2015 ; Ge et al, 2015 ; Li et al, 2015 ; Yao et al, 2015 ; Sulakhiya et al, 2016 ). In addition, this model has been modified in a variety of ways, including altering inflammatory agents ( Fischer et al, 2015 ), initiating chronic inflammation ( Kubera et al, 2013 ; Adzic et al, 2015 ; Gu an et al, 2015 ), or combining it with chronic stress exposure ( Elgarf et al, 2014 ) to study depression.…”

Section: Inflammation-induced Depressionmentioning

confidence: 99%

“…In addition, patients who attempted suicide have elevated quinolinic acid levels in the CSF compared with healthy controls ( Bay-Richter et al, 2014 ). In humans with traumatic brain injury, there is an increase in IDO and quinolinic acid in the CSF and brains of patients who had a worse recovery (Y an et al, 2015 ). Adding further evidence to a role for IDO and quinolinic acid in depression, the metabolites of kynurenine are elevated in depressed patients in the CSF without any corresponding change in CSF tryptophan ( Raison et al, 2010 ).…”

Section: Kynurenine Metabolitesmentioning

confidence: 99%

“…KMO catalyzes kynurenine into 3-HK and can be used to create quinolinic acid in microglia cells. Recently, KMO inhibitors have been proposed as potential therapeutic targets for Huntington’s disease (Toledo-Sherm an et al, 2015 ), and it may be worthwhile to explore these molecules in inflammation-induced depression. Kynurenine can alternatively produce kynurenic acid if it is metabolized by KATs instead of KMO, and because kynurenic acid has opposing roles of quinolinic acid, it could counteract its effects.…”

Section: Clinical Implications: Pharmacological Targets Beyond Inflammentioning

confidence: 99%

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Inflammation Models of Depression in Rodents: Relevance to Psychotropic Drug Discovery

Remus

Dantzer

2016

IJNPPY

136

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Inflammation and depression are closely inter-related; inflammation induces symptoms of depression and, conversely, depressed mood and stress favor an inflammatory phenotype. The mechanisms that mediate the ability of inflammation to induce symptoms of depression are intensively studied at the preclinical level. This review discusses how it has been possible to build animal models of inflammation-induced depression based on clinical data and to explore critical mechanisms downstream of inflammation. Namely, we focus on the ability of inflammation to increase the activity of the tryptophan-degrading enzyme, indoleamine 2,3 dioxygenase, which leads to the production of kynurenine and downstream neuroactive metabolites. By acting on glutamatergic neurotransmission, these neuroactive metabolites play a key role in the development of depression-like behaviors. An important outcome of the preclinical research on inflammation-induced depression is the identification of potential novel targets for antidepressant treatments, which include targeting the kynurenine system and production of downstream metabolites, altering transport of kynurenine into the brain, and modulating glutamatergic transmission.

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Effects of the total flavonoid extract of Xiaobuxin-Tang on depression-like behavior induced by lipopolysaccharide and proinflammatory cytokine levels in mice

Cited by 22 publications

References 35 publications

Role of the Kynurenine Metabolism Pathway in Inflammation-Induced Depression: Preclinical Approaches

Role of the Kynurenine Metabolism Pathway in Inflammation-Induced Depression: Preclinical Approaches

Inulin‐Type Oligosaccharides Extracted from Yacon Produce Antidepressant‐Like Effects in Behavioral Models of Depression

Inflammation Models of Depression in Rodents: Relevance to Psychotropic Drug Discovery

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