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Open AccessJournal ArticleDOI

P2X7 receptor activation aggravates NADPH oxidase 2-induced oxidative stress after intracerebral hemorrhage.

TLDR
In this paper, the effects of activated P2X7R-associated oxidative stress after intracerebral hemorrhage were investigated in mice, and the results indicated that activation aggravated NOX2-induced oxidative stress through the activation of the ERK1/2 and NF-κB pathways.
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This article is published in Neural Regeneration Research.The article was published on 2021-08-01 and is currently open access. It has received 17 citations till now. The article focuses on the topics: Intracerebral hemorrhage & Oxidative stress.

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Journal ArticleDOI

Inhibition of P2X4R attenuates white matter injury in mice after intracerebral hemorrhage by regulating microglial phenotypes.

TL;DR: In this article, the role of P2X4R in the WMI and the inflammatory response in mice, as well as the possible mechanism of action after ICH was investigated.
Journal ArticleDOI

NADPH Oxidases in the Central Nervous System: Regional and Cellular Localization and the Possible Link to Brain Diseases.

TL;DR: In this article, the significant role of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox) in signal transduction is mediated by the production of reactive oxygen species (ROS).
Journal ArticleDOI

The mechanism and relevant mediators associated with neuronal apoptosis and potential therapeutic targets in subarachnoid hemorrhage

TL;DR: The existing evidence on molecules and related drugs or molecules involved in the apoptotic pathway after SAH is summarized, which provides a possible target or new strategy for the treatment of SAH.
Journal ArticleDOI

Blocking P2RX7 Attenuates Ferroptosis in Endothelium and Reduces HG-induced Hemorrhagic Transformation After MCAO by Inhibiting ERK1/2 and P53 Signaling Pathways

TL;DR: In this paper , the authors explored the role of P2RX7 in reducing the pathogenesis of acute ischemic stroke through regulating endotheliocyte ferroptosis, which is a pattern of programmed cell death caused by the accumulation of intracellular iron and lipid peroxidation, resulting in ROS production and cell death.
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