Retinoic acid receptor agonist Am80 inhibits CXCL2 production from microglial BV-2 cells via attenuation of NF-κB signaling

Takaoka, Yuichiro; Takahashi, Moeka; Kurauchi, Yuki; Hisatsune, Akinori; Seki, Takahiro; Shudo, Koichi; Katsuki, Hiroshi

doi:10.1016/j.intimp.2016.06.025

Cited by 13 publications

(5 citation statements)

References 41 publications

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“…Reverse transcription–quantitative polymerase chain reaction (RT-qPCR) was conducted as previously described [ 25 ]. After drug treatment for the indicated periods, total RNA was extracted from cultured cells or slices using RNAiso plus (catalog No.…”

Section: Methodsmentioning

confidence: 99%

Aromatic-Turmerone Analogs Protect Dopaminergic Neurons in Midbrain Slice Cultures through Their Neuroprotective Activities

Hori

Tsutsumi

Nasu

et al. 2021

Cells

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Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra. The inflammatory activation of microglia participates in dopaminergic neurodegeneration in PD. Therefore, chemicals that inhibit microglial activation are considered to have therapeutic potential for PD. Aromatic (ar)-turmerone is a main component of turmeric oil extracted from Curcuma longa and has anti-inflammatory activity in cultured microglia. The aims of the present study are (1) to investigate whether naturally occurring S-enantiomer of ar-turmerone (S-Tur) protects dopaminergic neurons in midbrain slice cultures and (2) to examine ar-turmerone analogs that have higher activities than S-Tur in inhibiting microglial activation and protecting dopaminergic neurons. R-enantiomer (R-Tur) and two analogs showed slightly higher anti-inflammatory effects in microglial BV2 cells. S- and R-Tur and these two analogs reversed dopaminergic neurodegeneration triggered by microglial activation in midbrain slice cultures. Unexpectedly, this neuroprotection was independent of the inhibition of microglial activation. Additionally, two analogs more potently inhibited dopaminergic neurodegeneration triggered by a neurotoxin, 1-methyl-4-phenylpyridinium, than S-Tur. Taken together, we identified two ar-turmerone analogs that directly and potently protected dopaminergic neurons. An investigation using dopaminergic neuronal precursor cells suggested the possible involvement of nuclear factor erythroid 2-related factor 2 in this neuroprotection.

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Section: Methodsmentioning

confidence: 99%

Aromatic-Turmerone Analogs Protect Dopaminergic Neurons in Midbrain Slice Cultures through Their Neuroprotective Activities

Hori

Tsutsumi

Nasu

et al. 2021

Cells

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“…In the intracerebral hemorrhage (ICH) mice model, microglial activation in the perihematomal region is found within 1 h after ICH was induced. Molecular signals produced by M1 phenotype, such as IL-1β, TNF, and IL-6, and inducible nitric oxide synthase (iNOS) are amplified both in human and rodent perihematomal brain tissues ( Clausen et al, 2008 ; Wu et al, 2010 ; Liesz et al, 2011 ; Takaoka et al, 2016 ). Similarly, in the MCAO mice model, microglia are activated and invade the infarct core, simultaneously secreting cytokines IL-1β, TNF, and IL-1 receptor antagonist (IL-1Ra) ( Clausen et al, 2008 , 2016 ; Michelucci et al, 2009 ).…”

Section: Communication Between the Gs Cellular Componentsmentioning

confidence: 99%

The Glymphatic System: A Novel Therapeutic Target for Stroke Treatment

Zhao

et al. 2021

Front. Aging Neurosci.

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The glymphatic system (GS) is a novel defined brain-wide perivascular transit network between cerebrospinal fluid (CSF) and interstitial solutes that facilitates the clearance of brain metabolic wastes. The complicated network of the GS consists of the periarterial CSF influx pathway, astrocytes-mediated convective transport of fluid and solutes supported by AQP4 water channels, and perivenous efflux pathway. Recent researches indicate that the GS dysfunction is associated with various neurological disorders, including traumatic brain injury, hydrocephalus, epilepsy, migraine, and Alzheimer’s disease (AD). Meanwhile, the GS also plays a pivotal role in the pathophysiological process of stroke, including brain edema, blood–brain barrier (BBB) disruption, immune cell infiltration, neuroinflammation, and neuronal apoptosis. In this review, we illustrated the key anatomical structures of the GS, the relationship between the GS and the meningeal lymphatic system, the interaction between the GS and the BBB, and the crosstalk between astrocytes and other GS cellular components. In addition, we contributed to the current knowledge about the role of the GS in the pathology of stroke and the role of AQP4 in stroke. We further discussed the potential use of the GS in early risk assessment, diagnostics, prognostics, and therapeutics of stroke.

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“…RAR and RXR are DNA binding transcription factors and exert their influence through modulating target gene expression in the presence or absence of retinoids. Reported pathways associated with retinoid signaling include TGF, NFB (nuclear factor B), and Nrf2 (43)(44)(45). To understand the manner by which RAR and RXR reprogram cell state transitions, we performed chromatin immunoprecipitation sequencing (ChIP-seq) to identify their compendium of target genes in an unbiased manner.…”

Section: Lipid Metabolism Genes Are Regulated By Retinoid Receptorsmentioning

confidence: 99%

Fatty acid oxidation is a druggable gateway regulating cellular plasticity for driving metastasis in breast cancer

et al. 2021

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Retinoic acid receptor agonist Am80 inhibits CXCL2 production from microglial BV-2 cells via attenuation of NF-κB signaling

Cited by 13 publications

References 41 publications

Aromatic-Turmerone Analogs Protect Dopaminergic Neurons in Midbrain Slice Cultures through Their Neuroprotective Activities

Aromatic-Turmerone Analogs Protect Dopaminergic Neurons in Midbrain Slice Cultures through Their Neuroprotective Activities

The Glymphatic System: A Novel Therapeutic Target for Stroke Treatment

Fatty acid oxidation is a druggable gateway regulating cellular plasticity for driving metastasis in breast cancer

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