Nafamostat mesilate improves function recovery after stroke by inhibiting neuroinflammation in rats

Li, Chenhui; Wang, Jing; Fang, Yinquan; Liu, Yuan; Chen, Tao; Sun, Hao; Zhou, Xin‐Fu; Liao, Hong

doi:10.1016/j.bbi.2016.03.019

Cited by 48 publications

(39 citation statements)

References 35 publications

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“…Moreover, microglia tend to migrate from ischemic to perivascular areas in MCAO-treated animals, implying that ischemia strengthens their contact (Li et al, 2016). Yet, few reports have assessed the role of different microglial phenotypes in BBB function after ischemia.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: NOSH-NBP, a Novel Nitric Oxide and Hydrogen Sulfide- Releasing Hybrid, Attenuates Ischemic Stroke-Induced Neuroinflammatory Injury by Modulating Microglia Polarization

Xiang

et al. 2017

Front. Cell. Neurosci.

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NOSH-NBP, a novel nitric oxide (NO) and hydrogen sulfide (H2S)-releasing hybrid, protects brain from ischemic stroke. This study mainly aimed to investigate the therapeutic effect of NOSH-NBP on ischemic stroke and the underlying mechanisms. In vivo, transient middle cerebral artery occlusion (tMCAO) was performed in C57BL/6 mice, with NO-NBP and H2S-NBP as controls. NO and H2S scavengers, carboxy-PTIO and BSS, respectively, were used to quench NO and H2S of NOSH-NBP. In vitro, BV2 microglia/BMDM were induced to the M1/2 phenotype, and conditioned medium (CM) experiments in BV2 microglia, neurons and b.End3 cerebral microvascular endothelial cells (ECs) were performed. Microglial/macrophage activation/polarization was assessed by flow cytometry, Western blot, RT-qPCR, and ELISA. Neuronal and EC survival was measured by TUNEL, flow cytometry, MTT and LDH assays. Transmission electron microscopy, EB extravasation, brain water content, TEER measurement and Western blot were used to detect blood–brain barrier (BBB) integrity and function. Interestingly, NOSH-NBP significantly reduced cerebral infarct volume and ameliorated neurological deficit, with superior effects compared with NO-NBP and/or H2S-NBP in mice after tMCAO. Both NO and H2S-releasing groups contributed to protection by NOSH-NBP. Additionally, NOSH-NBP decreased neuronal death and attenuated BBB dysfunction in tMCAO-treated mice. Furthermore, NOSH-NBP promoted microglia/macrophage switch from an inflammatory M1 phenotype to the protective M2 phenotype in vivo and in vitro. Moreover, the TLR4/MyD88/NF-κB pathway and NLRP3 inflammasome were involved in the inhibitory effects of NOSH-NBP on M1 polarization, while peroxisome proliferator activated receptor gamma signaling contributed to NOSH-NBP induced M2 polarization. These findings indicated that NOSH-NBP is a potential therapeutic agent that preferentially promotes microglial/macrophage M1–M2 switch in ischemic stroke.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: NOSH-NBP, a Novel Nitric Oxide and Hydrogen Sulfide- Releasing Hybrid, Attenuates Ischemic Stroke-Induced Neuroinflammatory Injury by Modulating Microglia Polarization

Xiang

et al. 2017

Front. Cell. Neurosci.

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“…[45] The positive role associated with neuroinflammation is only present for a brief, controlled inflammatory situations and responses and this can be considered as performing a protective function to the host organism. [46][47][48] For example, during low transient inflammation that may occur during infections, the immune cell signals to the brain by increasing the expression of interleukin (IL)-1 cytokine, this then increasing the 'survellience' role of glia cells in the brain if infected. [49,50] The transient inflammation of traumatic CNS injury, following the expression of IL-4, has been shown to promote injury recovery and axonal regrowth.…”

Section: Neuroinflammationmentioning

confidence: 99%

Role of neuroinflammation in ischemic stroke

Li¹,

Pan²,

Tang³

et al. 2017

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Ischemic stroke causes the depletion of energy and induce excitotoxicity and neuroinflammation in the brain that results from thrombotic blockage. Neuroinflammation occurs initially depending on activated resident microglia that has the same function as the macrophage. Activated microglia participates in the neuroinflammatory process by phagocytosing the injured brain cells and producing the pro-and anti-inflammatory mediators. In this review, the authors present an overview of the role of microglia in mediating neuroinflammation in ischemic stroke. Key words:Microglia, ischemic stroke, neuroinflammation ABSTRACT Topic: StrokeThis is an open access article distributed under the terms of the Creative Commons AttributionNonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

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“…[17][18][19] Recent researches have demonstrated that NM can attenuate neuronal damage and improve functional recovery from CNS injuries such as shock and transient focal ischemia/reperfusion-induced brain injury in rats by decreasing infarct volume of brain edema, inhibiting neuroinflammation and other effects. [20][21][22] As serine protease activation occurs in SCI and triggers the inflammatory cascade, we hypothesized that NM treatment could attenuate inflammation and promote the repair of SCI.…”

Section: Introductionmentioning

confidence: 99%

Nafamostat mesilate attenuates inflammation and apoptosis and promotes locomotor recovery after spinal cord injury

Duan

Yao

et al. 2018

CNS Neurosci Ther

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Nafamostat mesilate improves function recovery after stroke by inhibiting neuroinflammation in rats

Cited by 48 publications

References 35 publications

RETRACTED: NOSH-NBP, a Novel Nitric Oxide and Hydrogen Sulfide- Releasing Hybrid, Attenuates Ischemic Stroke-Induced Neuroinflammatory Injury by Modulating Microglia Polarization

RETRACTED: NOSH-NBP, a Novel Nitric Oxide and Hydrogen Sulfide- Releasing Hybrid, Attenuates Ischemic Stroke-Induced Neuroinflammatory Injury by Modulating Microglia Polarization

Role of neuroinflammation in ischemic stroke

Nafamostat mesilate attenuates inflammation and apoptosis and promotes locomotor recovery after spinal cord injury

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