Publications by authors named "Xialin Tang"

Autophagy plays a pivotal role in the pathogenesis and progression of Alzheimer's disease (AD). Oxidative stress and neuroinflammation involved in autophagy are associated with the cerebral ischemia-induced exacerbation of cognitive deficits in individuals with AD. APP/PS1 mice underwent bilateral common carotid artery clamping for 15 min.

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  • * A new test, called the time-resolved fluorescence immunochromatographic test strip (TRFIS), was developed that can quickly and accurately measure serum GFAP levels, showing a wide detection range and sensitivity.
  • * The TRFIS demonstrated high specificity and precision, successfully differentiating between healthy individuals and those with cerebral hemorrhage, making it a valuable tool for on-site TBI diagnosis.
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  • DDX5 is identified as a negative regulator of type I interferon (IFN-I) production during antiviral responses, meaning it suppresses the immune response to viruses.
  • Knocking down DDX5 increases the production of IFN-I and the expression of IFN-stimulated genes (ISGs) in response to viral infections, whereas overexpressing DDX5 does the opposite.
  • The study shows that DDX5 interacts with PP2A-Cβ, which regulates IRF3, a key factor in the IFN-I signaling pathway, thus revealing how DDX5 affects antiviral immunity.
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Background: Long non-coding RNAs (LncRNAs) have been reported to play important roles in the pathogenesis and development of many diseases, including cerebral ischemia and reperfusion (I/R) injury. In this study, we aimed to investigate the role of LncRNA-Potassium Voltage-Gated Channel Subfamily Q Member 1 opposite strand/antisense transcript 1 (KCNQ1OT1) in cerebral I/R induced neuronal injury, and its underlying mechanisms.

Methods: Primary mouse cerebral cortical neurons treated with oxygen-glucose deprivation and reoxygenation (OGD/R) in vitro and mice subjected to middle cerebral artery occlusion (MCAO) and reperfusion were used to mimic cerebral I/R injury.

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  • Ischemic stroke is a major cause of death globally, with inflammation playing a critical role in its progression; this study investigates the role of microRNA-421-3p in inflammation during cerebral ischemia/reperfusion (I/R) injury.
  • Researchers used both animal and cell models to study the effects of microRNA-421-3p, employing various scientific techniques to assess its influence on I/R injury and inflammation mechanisms.
  • The findings indicate that microRNA-421-3p levels decrease during I/R injury, and its overexpression reduces inflammation by targeting the YTHDF1 protein, which subsequently affects the translation of the pro-inflammatory NF-κB p65 protein.
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Aim And Objective: Cell death is a main pathological change in brain ischemia. Astragalus membranaceus (Ast) and ligustrazine (Lig), as traditional Chinese herbs, have a protective effect against ischemia-reperfusion injury. We aim to find whether the underlying protective mechanism of Astragalus membranaceus and ligustrazine against Oxygen-glucose deprivation/reoxygenation (OGD/R) -induced injury in RBMECs is related to PKCδ/MARCKS pathway.

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(Ast) and ligustrazine (Lig) have a protective effect on lower hemorrhagic transformation induced by pharmaceutical thrombolysis. The cerebral ischemia rat model was induced with autologous blood clot injections. A combination of Ast and Lig, or a protein kinase C delta (PKCδ) inhibitor-rottlerin, or a combination of Ast, Lig, and rottlerin was administered immediately after recombinant tissue plasminogen activator injection.

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The purpose of the study was to evaluate the effect of extract and ligustrazine combination on ameliorating inflammation in cerebral ischemic rats that have undergone thrombolysis. and ligustrazine per se, or a combination of and ligustrazine was administered by intraperitoneal injection immediately after surgery and sham surgery. After the induction of thrombolysis, the neurological function was measured and cerebral lesion volume was determined.

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Yin-Yang 1 (YY1) has been identified as playing critical roles in multiple diseases. However, little is known regarding its roles and mechanisms in cerebral ischemia/reperfusion (I/R) injury. This study is aimed to explore the roles of YY1 in regulating neuronal apoptosis in cerebral I/R injury and its underlying mechanisms.

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