MCP-1-deficient mice show reduced neuroinflammatory responses and increased peripheral inflammatory responses to peripheral endotoxin insult

Thompson, Wendy L.; Karpus, William J.; Eldik, Linda J. Van

doi:10.1186/1742-2094-5-35

Cited by 86 publications

(73 citation statements)

References 49 publications

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“…The bacterial endotoxin also markedly increased TNF-a in brain. Other studies have indicated decreased brain GSH and glutathione reductase activity, cyclooxygenase-2 expression, lipid peroxidation, impairment in mitochondrial redox activity (Noble et al 2007;Jacewicz et al 2009), as well as increased production of pro-inflammatory cytokines, such as IL-1b and TNF-a, in the brain and periphery (Buttini et al 1997;Fiorucci et al 2002;Thompson et al 2008) after systemic LPS administration in rodents. In LPS-treated mice, the administration of aspartame resulted in further increase in oxidative stress in brain (though not in the liver), suggesting that the latter is more susceptible to the effect of aspartame.…”

Section: Discussionmentioning

confidence: 96%

Effect of Aspartame on Oxidative Stress and Monoamine Neurotransmitter Levels in Lipopolysaccharide-Treated Mice

2011

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This study aimed at investigating the effect of the sweetener aspartame on oxidative stress and brain monoamines in normal circumstances and after intraperitoneal (i.p.) administration of lipopolysaccharide (LPS; 100 μg/kg) in mice. Aspartame (0.625-45 mg/kg) was given via subcutaneous route at the time of endotoxin administration. Mice were euthanized 4 h later. Reduced glutathione (GSH), lipid peroxidation (thiobarbituric acid-reactive substances; TBARS), and nitrite concentrations were measured in brain and liver. Tumor necrosis factor-alpha (TNF-α) and glucose were determined in brain. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were measured in liver. The administration of only aspartame (22.5 and 45 mg/kg) increased brain TBARS by 17.7-32.8%, decreased GSH by 25.6-31.6%, and increased TNF-α by 16.7-44%. Aspartame caused dose-dependent inhibition of brain serotonin, noradrenaline, and dopamine. Aspartame did not alter liver TBARS, nitrite, GSH, AST, ALT, or ALP. The administration of LPS increased nitrite in brain and liver by 26.8 and 37.1%, respectively; decreased GSH in brain and liver by 21.6 and 31.1%, respectively; increased brain TNF-α by 340.4%, and glucose by 39.9%, and caused marked increase in brain monoamines. LPS increased AST, ALT, and ALP in liver tissue by 84.4, 173.7, and 258.9%, respectively. Aspartame given to LPS-treated mice at 11.25 and 22.5 mg/kg increased brain TBARS by 15.5-16.9%, nitrite by 12.6-20.1%, and mitigated the increase in monoamines. Aspartame did not alter liver TBARS, nitrite, GSH, ALT, AST, or ALP. Thus, the administration of aspartame alone or in the presence of mild systemic inflammatory response increases oxidative stress and inflammation in the brain, but not in the liver.

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Section: Discussionmentioning

confidence: 96%

Effect of Aspartame on Oxidative Stress and Monoamine Neurotransmitter Levels in Lipopolysaccharide-Treated Mice

2011

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“…3A). Based on the chemoattractant properties of the CCR2/CCL2 signaling (Thompson et al, 2008;Mildner et al, 2009), CCR2 upregulation on both microglia and brain macrophages by EE may suggest that EE could make these cells more responsive and more mobile with respect to future eventual injuries.…”

Section: Discussionmentioning

confidence: 99%

Enriched environment decreases microglia and brain macrophages inflammatory phenotypes through adiponectin-dependent mechanisms: Relevance to depressive-like behavior

Chabry

Nicolas

Cazareth

et al. 2015

Brain, Behavior, and Immunity

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“…Stimulation with LPS can induce the expression of iNOS, COX-2, pro-inflammatory cytokines and chemokines in microglial cells (Saud et al, 2005;Thompson et al, 2008;Kao et al, 2010;Lu et al, 2010). Several lines of evidence suggest that microglial cells can secrete pro-inflammatory cytokines, such as IL-1β, IL-6, IFNγ and TNF-α, which in turn, can act on these cells in an autocrine manner (Graeber and Streit, Cell viability assay using CCK-8 kit was examined at 24 h following treatment with visnagin (0, 5, 10, 25, 50 and 100 µM).…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory effect of visnagin in lipopolysaccharide-stimulated BV-2 microglial cells

et al. 2010

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Visnagin, which is found in Ammi visnaga, has biological activity as a vasodilator and reduces blood pressure by inhibiting calcium influx into the cell. The present study demonstrates the anti-inflammatory effect of visnagin on lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. When cells were treated with visnagin prior to LPS stimulation, production of nitric oxide and expression of iNOS were attenuated in a dose-dependent manner. Visnagin also caused a significant decrease of mRNA expression and release of TNF-α, IL-1β and IFNγ. In addition, visnagin reduced LPS-induced IL-6 and MCP-1 mRNA level. We further found that visnagin dose-dependently inhibited LPS-induced AP-1 and NF-κB luciferase activities. Taken together, our results for the first time suggest that the anti-inflammatory effect of visnagin might result from the inhibition of transcription factors, such as AP-1 and NF-κB.

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MCP-1-deficient mice show reduced neuroinflammatory responses and increased peripheral inflammatory responses to peripheral endotoxin insult

Cited by 86 publications

References 49 publications

Effect of Aspartame on Oxidative Stress and Monoamine Neurotransmitter Levels in Lipopolysaccharide-Treated Mice

Effect of Aspartame on Oxidative Stress and Monoamine Neurotransmitter Levels in Lipopolysaccharide-Treated Mice

Enriched environment decreases microglia and brain macrophages inflammatory phenotypes through adiponectin-dependent mechanisms: Relevance to depressive-like behavior

Anti-inflammatory effect of visnagin in lipopolysaccharide-stimulated BV-2 microglial cells

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