Comparison of chicoric acid, and its metabolites caffeic acid and caftaric acid: In vitro protection of biological macromolecules and inflammatory responses in BV2 microglial cells

Abstract Six hydroxycinnamic acids : caffeic acid, chlorogenic acid, 3,5-O-dicaffeoylquinic acid 2-O-caffeoyltartaric acid (caftaric acid) and 2,3-O-dicaffeoyltartaric acid (chicoric acid) have been isolated from Lapsana communis L. subsp. communis aerial parts. Among flavonoids, only isoquercitrin, luteolin and luteolin-7-O-β-glucuronide were identified. Except for chlorogenic acid, these com pounds represent the first report in Lapsana communis. Chicoric acid is the major phenylpropanoic constituent in this plant.

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Interferon Regulatory Factor 5 Mediates Lipopolysaccharide-Induced Neuroinflammation

Frontiers in Immunology ◽

10.3389/fimmu.2020.600479 ◽

2020 ◽

Vol 11 ◽

Author(s):

Ziqi Fan ◽

Shuai Zhao ◽

Yueli Zhu ◽

Zheyu Li ◽

Zhirong Liu ◽

...

Keyword(s):

Inflammatory Cytokines ◽

Inflammatory Responses ◽

Interferon Regulatory Factor ◽

Microglial Cells ◽

Regulatory Factor ◽

Down Regulation ◽

Interferon Regulatory Factor 5 ◽

Bv2 Microglial Cells ◽

Lps Treatment ◽

Pro Inflammatory Cytokines

BackgroundActivated microglia play a vital role in neuroinflammation in the central nervous system (CNS), which is associated with the pathogenesis and the progression of neurological diseases. Interferon regulatory factor 5 (IRF5) has been well established participating in inflammatory responses and is highly expressed in M1 macrophage in the periphery, the role of which in the CNS remains elusive.MethodsLipopolysaccharide (LPS) was employed to induce neuroinflammation. Down-regulation of IRF5 in C57/BL6 mice and BV2 microglial cells were achieved by IRF5 siRNA transfection. The levels of pro-inflammatory cytokines were evaluated by ELISA and quantitative real-time PCR. The expression levels of IRF5 were examined by immunofluorescence and Western blot.ResultsLPS induced significantly elevated expression of IRF5 in mouse brain, which co-localized with CD11b-positive microglia. Down-regulation of IRF5 quenched the pro-inflammatory responses. The levels of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 were up-regulated at 4 h after LPS treatment, which were significantly down-regulated with the knockdown of IRF5. LPS-induced pro-inflammatory responses were transient, which were comparable to control group at 24 h after LPS treatment. However, LPS did not up-regulate the expression of IRF5 in BV2 microglial cells, indicating that LPS-induced inflammation in BV2 cells does not involve IRF5 signaling.ConclusionsIRF5 mediates the inflammatory responses in the CNS, which might serve as a therapeutic target for CNS inflammatory diseases. LPS-induced inflammation does not involve IRF5 signaling in BV2 microglia.

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Mucuna pruriens (L.) DC. seed extract inhibits lipopolysaccharide-induced inflammatory responses in BV2 microglial cells

Journal of Ethnopharmacology ◽

10.1016/j.jep.2020.113518 ◽

2021 ◽

Vol 267 ◽

pp. 113518

Author(s):

Aungkana Rachsee ◽

Natthakarn Chiranthanut ◽

Phraepakaporn Kunnaja ◽

Seewaboon Sireeratawong ◽

Parirat Khonsung ◽

...

Keyword(s):

Inflammatory Responses ◽

Seed Extract ◽

Microglial Cells ◽

Mucuna Pruriens ◽

Bv2 Microglial Cells

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Hypoxia Potentiates LPS-Mediated Cytotoxicity of BV2 Microglial Cells In Vitro by Synergistic Effects on Glial Cytokine and Nitric Oxide System

Neuropediatrics ◽

10.1055/s-0035-1562924 ◽

2015 ◽

Vol 46 (05) ◽

pp. 321-328 ◽

Cited By ~ 7

Author(s):

Florian Brackmann ◽

Mandy Richter-Kraus ◽

Regina Trollmann ◽

Daniel Frey ◽

Susan Jung

Keyword(s):

Nitric Oxide ◽

Synergistic Effects ◽

Oxide System ◽

Microglial Cells ◽

Bv2 Microglial Cells ◽

Nitric Oxide System

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Regulation of inflammatory responses by neuregulin-1 in brain ischemia and microglial cells in vitro involves the NF-kappa B pathway

Journal of Neuroinflammation ◽

10.1186/s12974-016-0703-7 ◽

2016 ◽

Vol 13 (1) ◽

Cited By ~ 54

Author(s):

Lauren J. Simmons ◽

Monique C. Surles-Zeigler ◽

Yonggang Li ◽

Gregory D. Ford ◽

Gale D. Newman ◽

...

Keyword(s):

Brain Ischemia ◽

Inflammatory Responses ◽

Microglial Cells ◽

Nf Kappa B ◽

Neuregulin 1

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Dectin-1/Syk signaling triggers neuroinflammation after ischemic stroke in mice

10.21203/rs.2.17199/v2 ◽

2019 ◽

Author(s):

Xin-chun Ye ◽

Qi Hao ◽

Wei-jing Ma ◽

Qiu-chen Zhao ◽

Wei-wei Wang ◽

...

Keyword(s):

Ischemic Stroke ◽

Brain Injury ◽

Infarct Volume ◽

Inos Expression ◽

Microglial Cells ◽

Brain Infarct ◽

Tnf Α ◽

Bv2 Microglial Cells ◽

The Brain

Abstract Dendritic cell-associated C-type lectin-1 (Dectin-1) receptor has been reported to be involved in neuroinflammation in Alzheimer's disease and traumatic brain injury. The present study was designed to investigate the role of Dectin-1 and its downstream target spleen tyrosine kinase (Syk) in early brain injury after ischemic stroke using a focal cortex ischemic stroke model. Adult male C57BL/6J mice were subjected to a cerebral focal ischemia model of ischemic stroke. The neurological score, adhesive removal test and foot-fault test were evaluated on days 1, 3, 5 and 7 after ischemic stroke. Dectin-1, Syk, phosphorylated (p)-Syk, tumor necrosis factor-α (TNF-α) and inducible nitric oxide synthase (iNOS) expression was analyzed via western blotting in ischemic brain tissue after ischemic stroke and in BV2 microglial cells subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) injury in vitro. The brain infarct volume and Iba1-positive cells were evaluated using Nissl’s and immunofluorescence staining, respectively. The Dectin-1 antagonist laminarin (LAM) and a selective inhibitor of Syk phosphorylation (piceatannol; PIC) were used for the intervention. Dectin-1, Syk, and p-Syk expression was significantly enhanced on days 3, 5 and 7 and peaked on day 3 after ischemic stroke. The Dectin-1 antagonist LAM or Syk inhibitor PIC decreased the number of Iba1-positive cells and TNF-α and iNOS expression, decreased the brain infarct volume and improved neurological functions on day 3 after ischemic stroke. In addition, the in vitro data revealed that Dectin-1, Syk and p-Syk expression was increased following the 3-h OGD and 0, 3 and 6 h of reperfusion in BV2 microglial cells. LAM and PIC also decreased TNF-α and iNOS expression 3 h after OGD/R induction. Dectin-1/Syk signaling plays a crucial role in inflammatory activation after ischemic stroke, and further investigation of Dectin-1/Syk signaling in stroke is warranted.

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Interferon Regulatory Factor 5 Mediates Lipopolysaccharide Induced Neuroinflammation

10.21203/rs.3.rs-23387/v1 ◽

2020 ◽

Author(s):

Ziqi Fan ◽

Shuai Zhao ◽

Yueli Zhu ◽

Zheyu Li ◽

Zhirong Liu ◽

...

Keyword(s):

Inflammatory Cytokines ◽

Inflammatory Responses ◽

Interferon Regulatory Factor ◽

Microglial Cells ◽

Regulatory Factor ◽

Down Regulation ◽

Interferon Regulatory Factor 5 ◽

Bv2 Microglial Cells ◽

Lps Treatment ◽

Pro Inflammatory Cytokines

Abstract Background Activated microglia plays a vital role in neuroinflammation in central nervous system (CNS), which is associated with the pathogenesis and the progression of neurological diseases. Interferon regulatory factor 5 (IRF5) has been well established participating in inflammatory responses and is highly expressed in M1 macrophage in periphery, the role of which in the CNS remains elusive. Methods Lipopolysaccharide (LPS) was employed to induce neuroinflammation. Down-regulation of IRF5 in C57/BL6 mice and BV2 microglial cells were achieved by IRF5 siRNA transfection. The levels of pro-inflammatory cytokines were evaluated by ELISA and quantitative real-time PCR. The expression levels of IRF5 were examined by immnunofluorescence and Western blot. Results LPS induced significantly elevated expression of IRF5 in mouse brain, which co-localized with CD11b positive microglia. Down-regulation of IRF5 quenched the pro-inflammatory responses. The levels of pro-inflammatory cytokines TNF-α, IL-1β and IL-6 were up-regulated at 4 h after LPS treatment, which were significantly down-regulated with the knockdown of IRF5. LPS-induced pro-inflammatory responses were transient, which returned to basal level at 24 h after LPS treatment. However, LPS did not up-regulate the expression of IRF5 in BV2 microglial cells, indicating that LPS-induced inflammation in BV2 cells does not involve IRF5 signaling. Conclusions IRF5 mediates the inflammatory responses in the CNS, which might serve as a therapeutic target for CNS inflammatory diseases. LPS-induced inflammation does not involve IRF5 signaling in BV2 microglia.

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Fowlerstefin, a cysteine protease inhibitor of Naegleria fowleri, induces inflammatory responses in BV-2 microglial cells in vitro

Parasites & Vectors ◽

10.1186/s13071-020-3909-6 ◽

2020 ◽

Vol 13 (1) ◽

Author(s):

Thị Lam Thái ◽

Jung-Mi Kang ◽

Hương Giang Lê ◽

Jinyoung Lee ◽

Won Gi Yoo ◽

...

Keyword(s):

Protease Inhibitor ◽

Cysteine Protease ◽

Inflammatory Responses ◽

Microglial Cells ◽

Cysteine Protease Inhibitor ◽

Naegleria Fowleri ◽

Nægleria Fowleri

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Aquilariae Lignum Methylene Chloride Fraction Attenuates IL-1β-Driven Neuroinflammation in BV2 Microglial Cells

International Journal of Molecular Sciences ◽

10.3390/ijms21155465 ◽

2020 ◽

Vol 21 (15) ◽

pp. 5465

Author(s):

Jin-Seok Lee ◽

Yoo-Jin Jeon ◽

Ji-Yun Kang ◽

Sam-Keun Lee ◽

Hwa-Dong Lee ◽

...

Keyword(s):

Methylene Chloride ◽

Underlying Mechanism ◽

Microglial Cells ◽

Bv2 Cells ◽

Tnf Α ◽

Underlying Mechanisms ◽

Bv2 Microglial Cells ◽

Methylene Chloride Fraction

Microglial hyperactivation and neuroinflammation are known to induce neuronal death, which is one of the main causes of neurodegenerative disorders. We previously found that Aquilariae Lignum extract attenuated both neuronal excitotoxicity and neuroinflammation in vivo and in vitro. For further analysis, we extracted the methylene chloride fraction of Aquilariae Lignum to determine the bioactive compounds. In this study, we investigated the anti-neuroinflammatory effects and underlying mechanisms of the Aquilariae Lignum fraction (ALF) using lipopolysaccharide (LPS)-stimulated BV2 microglial cells. BV2 cells were pretreated with ALF (0.5, 1, and 2.5 μg/mL) before treatment with LPS (1 μg/mL). Pretreatment with ALF significantly attenuated the LPS-induced overproductions of nitric oxide (NO), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and interleukin (IL)-1β. These anti-inflammatory effects were supported by ALF-mediated modulation of the nuclear factor-kappa B (NF-κB) pathway. Furthermore, ALF exerted strong anti-inflammasome effects, as shown by IL-1β-specific inhibitory activity, but not activity against tumor necrosis factor (TNF)-α, along with inhibition of caspase-1 activity and NACHT, LRR, and PYD domain-containing protein 3 (NLRP3)-related molecules. These results indicate the potent anti-neuroinflammatory activity of ALF and that its underlying mechanism may involve the regulation of NLRP3 inflammasome-derived neuroinflammation in microglial cells.

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