Glycogen synthase kinase-3β regulates anti-inflammatory property of fluoxetine

Su, Hui; Ting, Ching Heng; Yu, Bu Chin; Chien, Yu Chieh; Tsai, Cheng‐Chieh; Huang, Wei-Ching; Lin, Chiou Feng; Chuang, Yeu-Hui; Young, Kung Chia; Wang, Jieh Neng; Tsao, Chiung Wen

doi:10.1016/j.intimp.2012.06.015

Cited by 37 publications

(24 citation statements)

References 45 publications

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“…Fluoxetine acts directly on peripheral cells that participate in the inflammatory response. This observation has been noted in animal models of rheumatoid arthritis, 18 allergic asthma, 15 lipopolysaccharide‐induced inflammation, 39 and septic shock 15 …”

Section: Discussionmentioning

confidence: 63%

Effect of Fluoxetine on Periodontal Status in Patients With Depression: A Cross‐Sectional Observational Study

Bhatia

Sharma

Tewari

et al. 2015

Journal of Periodontology

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Section: Discussionmentioning

confidence: 63%

Effect of Fluoxetine on Periodontal Status in Patients With Depression: A Cross‐Sectional Observational Study

Bhatia

Sharma

Tewari

et al. 2015

Journal of Periodontology

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“…Since effect of paroxetine on IL-6 was neither mediated via 5-HT receptor nor by GRK2 inhibition, other mechanisms are likely at play. In this regard, a recent study showed that fluoxetine's inhibitory effect on LPS-induced iNOS/NO release and COX-2/PGE2 production are dependent on GSK3β in macrophages[38]. …”

Section: Discussionmentioning

confidence: 99%

Paroxetine differentially modulates LPS-induced TNFα and IL-6 production in mouse macrophages

Durairaj

Steury

Parameswaran

2015

International Immunopharmacology

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Paroxetine is a selective serotonin reuptake inhibitor (SSRI) that is clinically used for the treatment of depression in human patients. Because of recent reports on the role of serotonin in modulating inflammation and the link between inflammation and depression, we sought to test the effect of paroxetine directly on macrophage response to an inflammatory stimulus. Lipopolysaccharide (LPS) treatment of mouse macrophages significantly enhanced TNFα and IL-6 production. Paroxetine treatment of macrophages however, significantly inhibited LPS-induced IL-6 production. In contrast, paroxetine enhanced LPS-induced TNFα production in macrophages. These effects of paroxetine were mimicked by fluoxetine, another SSRI. To determine if the effects of paroxetine are mediated via modulation of the 5-HT system, we treated macrophages with 5-HT or 5-HT receptor antagonist (LY215840) in the presence of LPS and/or paroxetine. 5-HT treatment by itself did not affect LPS-induced cytokine production. LY215840 however, reversed paroxetine's effect on LPS-induced TNFα production but not IL-6. To understand the signaling mechanisms, we examined paroxetine's effect on MAPK and NFκB pathways. While paroxetine inhibited LPS-induced IκBα phosphorylation, MAPK pathways were mostly unaffected. Together these data demonstrate that paroxetine has critical but differential effects on IL-6 and TNFα production in macrophages and that it likely regulates these cytokines via distinct mechanisms.

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“…Generally, under an AKT -activated process, complete activation requires Ser473, so levels of Ser473 phosphorylation represent the degree of AKT phosphorylation. GSK-3β is rendered inactive when it is phosphorylated at Ser9 by activated AKT [33]. Schematic structures of human AKT 1 and GSK-3β protein are shown in Figure 2.…”

Section: Tau Phosphorylation Involved In the Pi3k/akt/gsk-3β Signalinmentioning

confidence: 99%

Dietary regulation of PI3K/AKT/GSK-3β pathway in Alzheimer’s disease

Kitagishi

Nakanishi

Ogura

et al. 2014

Alzheimers Res Ther

172

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Alzheimer’s disease (AD) is characterized by the formation of senile plaques and neurofibrillary tangles composed of phosphorylated Tau. Several findings suggest that correcting signal dysregulation for Tau phosphorylation in AD may offer a potential therapeutic approach. The PI3K/AKT/GSK-3β pathway has been shown to play a pivotal role in neuroprotection, enhancing cell survival by stimulating cell proliferation and inhibiting apoptosis. This pathway appears to be crucial in AD because it promotes protein hyper-phosphorylation in Tau. Understanding those regulations may provide a better efficacy of new therapeutic approaches. In this review, we summarize advances in the involvement of the PI3K/AKT/GSK-3β pathways in cell signaling of neuronal cells. We also review recent studies on the features of several diets and the signaling pathway involved in AD.

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Glycogen synthase kinase-3β regulates anti-inflammatory property of fluoxetine

Cited by 37 publications

References 45 publications

Effect of Fluoxetine on Periodontal Status in Patients With Depression: A Cross‐Sectional Observational Study

Effect of Fluoxetine on Periodontal Status in Patients With Depression: A Cross‐Sectional Observational Study

Paroxetine differentially modulates LPS-induced TNFα and IL-6 production in mouse macrophages

Dietary regulation of PI3K/AKT/GSK-3β pathway in Alzheimer’s disease

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