Fluoxetine shows neuroprotective effects against LPS-induced neuroinflammation via the Notch signaling pathway

Zhang, Jing; Zhang, Naiwen; Lei, Jianfeng; Jing, Bin; Li, Mengyuan; Tian, Huiling; Xue, Bing; Li, Xiaoli

doi:10.1016/j.intimp.2022.109417

Cited by 17 publications

(5 citation statements)

References 58 publications

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“… 38 A recent study also suggested that Fluoxetine has neuroprotective effects in relieving lipopolysaccharide (LPS)-induced depression-like and motor behaviors by inhibiting the expression of Hes5. 39 These findings are consistent with the results of this study, which demonstrated that the Notch3-Hes5 signaling pathway may be involved in the effect of propofol on memory processing.…”

Section: Discussionsupporting

confidence: 92%

Effects of Subchronic Propofol Administration on the Proliferation and Differentiation of Neural Stem Cells in Rat Hippocampus

Chang

Bai

et al. 2023

Current Therapeutic Research

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Section: Discussionsupporting

confidence: 92%

Effects of Subchronic Propofol Administration on the Proliferation and Differentiation of Neural Stem Cells in Rat Hippocampus

Chang

Bai

et al. 2023

Current Therapeutic Research

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“…In this study, we con rmed that miR-135b-5p could target Pidd1, that was, circMap2k1 level was elevated in the MCAO group, and the inhibition of Pidd1 by miR-135b-5p was removed by molecular sponge adsorption. Zhang J et al demonstrated that uoxetine could improve brain activity and white matter ber injury, reduce Iba-1 expression in prefrontal cortex, hippocampus and substantia nigra, and reduce in ammatory factors IL-1α, IL-6 and TNF-α levels [42]. We found that in MCAO group, high expression of circMap2k1 caused an increase in the expression of Pidd1, which in turn led to an increase in microglia marker Iba-1 expression, that was, microglia were activated in the model group, and the activation of microglia could induce in ammatory factors release and further promote nerve cells apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of fluoxetine downregulation of circMap2k1 to alleviate neurological function after ischemic stroke

Zhang,

Deng,

et al. 2023

Preprint

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Background Ischemic stroke (IS) is known for its high incidence, disability and mortality, and there is an urgent need to investigate the pathophysiological mechanisms and develop novel treatment strategies. We aimed to investigate the mechanisms of the novel circMap2k1/miR-135b-5p/Pidd1 axis in the treatment of IS progression with fluoxetine. Methods The middle cerebral artery occlusion (MCAO) model was established, followed by fluoxetine treatment and injecting adeno-associated viruses (AAV)-sh-ctr and AAV-sh-circMap2k1 into bilateral hippocampal tissues of rats. Then cerebral infarction area, weight, Longa score, and neurological injury were evaluated. Dual-luciferase reporter gene assay was employed to confirm the binding between miR-135b-5p and Pidd1. ELISA was performed to measure the concentrations of inflammatory factors TNF-α, IL-6, and IL-1β in the plasma. Finally, we verified the role of circMap2k1 in cellular experiments by overexpression of circMap2k1. Cell viability was assessed using CCK-8 assay, while apoptosis was measured by flow cytometry. Results Knockdown of circMap2k1 enhanced the therapeutic effect of fluoxetine on IS injury (cerebral infarction area, weight, and Longa score) in rats. Then knockdown of circMap2k1 enhanced the protective effect of fluoxetine on neurological injury after IS in rats. Dual-luciferase reporter gene assay confirmed the targeting of miR-135b-5p to Pidd1. Additionally, fluoxetine deactivated the adsorption of miR-135b-5p by downregulating circMap2k1, and miR-135b-5p further exerts its inhibitory effect on Pidd1, and finally attenuares the inflammatory response caused by microglial polarization after IS. Cell experiments revealed that overexpression of circMap2k1 repressed cell viability and promoted cell apoptosis. Conclusions Fluoxetine downregulated circMap2k1 to ameliorate neurological injury and inflammatory responses induced by microglia polarization after IS.

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“…Because AAK1 localized to neurons to mediate clathrin-dependent endocytosis (46) which was included in our top enriched pathways among all upregulated mRNAs (see Figure 1d). In addition, AAK1 was involved in Notch signaling pathway (see Table S5), which has been proven to be related to the pathogenesis of depression (47,48). AC156455.1 and miR-126-5p formed a regulatory axis with AAK1 in the network based on bioinformatics prediction.…”

Section: Establishment Of Two Lncrna-mirna-mrna Networkmentioning

confidence: 99%

Aberrant plasma exosomal derived ceRNA networks as diagnosis biomarkers for adolescent major depressive disorder and its potential prediction for antidepressant

Liu

et al. 2023

Preprint

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Background: Major depressive disorder (MDD) in adolescence seriously endangers their mental and physical health and is associated with poor social and scholastic function. However, the diagnosis biomarkers for adolescent with MDD remain unclear. Methods：A total of 114 adolescent subjects were enrolled in this study, the comprehensive clinical and cognitive assessments were performed. Differential expressions of lncRNAs and mRNAs of plasma exosomes were screened by microarray assay. Two sets of ceRNA (lncRNAs-miRNAs-mRNAs) networks had been generated and candidate genes had been screened by bioinformatic analysis, and candidate genes were validated in cohort using qRT-PCR. Results：A total of 3752 differentially expressed lncRNAs and 1789 differentially expressed mRNAs were identified. AC156455.1, miR-126-5p, AAK1 and CCDC18AS1, miR-6835-5p, CCND2 were picked from each network as candidate genes. We found that the six candidate genes were differential expression between MDD patients and healthy controls, or before and after antidepressant treatment of MDD group. The expression levels of AAK1, CCDC18AS1 and miR6835 varied in efficacy after 8-week sertraline treatment. We also found that the expression of CCDC18AS1, miR-6835-5p, CCND2 (in the same network) at baseline could predicted antidepressant efficacy, which may be mediated through reducing suicidal ideation and improving cognitive function. Conclusion:Our study identified and validated the plasma exosome-derived ceRNA networks altered in adolescent with MDD, our findings provided potential diagnosis and therapeutic biomarkers for adolescent with MDD.

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Fluoxetine shows neuroprotective effects against LPS-induced neuroinflammation via the Notch signaling pathway

Cited by 17 publications

References 58 publications

Effects of Subchronic Propofol Administration on the Proliferation and Differentiation of Neural Stem Cells in Rat Hippocampus

Effects of Subchronic Propofol Administration on the Proliferation and Differentiation of Neural Stem Cells in Rat Hippocampus

Mechanism of fluoxetine downregulation of circMap2k1 to alleviate neurological function after ischemic stroke

Aberrant plasma exosomal derived ceRNA networks as diagnosis biomarkers for adolescent major depressive disorder and its potential prediction for antidepressant

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