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Chongqing, China

Wu X.,Chongqing Medical University | Li W.,Chongqing Medical University | Zhang G.,Jiangjin Center Hospital | Zhang Q.,Chongqing the Fourth Hospital | Cheng Y.,Chongqing Medical University
Analytical Methods | Year: 2014

Traumatic brain injury (TBI) has been associated with an acute stress response mediated by the sympathoadrenomedullary axis, which can be assessed by measuring glucose levels. Thus, aiming for a more convenient assay system of glucose, a novel electrochemical measurement for the sensitive detection of glucose in cerebrospinal fluid (CSF) was developed in this work in virtue of the electrodeposition of platinum nanoclusters on stable composite films constructed from carbon nanotubes (CNTs) and a core-shell organosilica@chitosan nanospheres (OrgSi@CS) modified glassy carbon electrode. The morphologies and the structures of the OrgSi@CS-CNTs composite material and platinum nanoclusters were characterized by atomic force microscopy (AFM), transmission electron microscopy (TEM) and X-ray photoelectron spectroscopy (XPS). Cyclic voltammetries (CVs) were used to investigate the direct electrochemistry behavior between the electroactive center of glucose oxidase (GOD) and the electrode. The linear response range was determined from 1.2 × 10-6 to 1.6 × 10-3 M with a detection limit of 4.0 × 10-7 M, and the Michaelis-Menten constant (KappM) value was estimated to be 0.41 mM, indicating a high-catalytic activity for glucose. In vitro experiments were performed with clinical samples of CSF obtained from TBI patients and compared with the glucose oxidase endpoint method, which showed an acceptable measurement with enhanced speed and convenience, indicating the feasibility of the sensors for a real-time continuous monitoring in vivo. © The Royal Society of Chemistry 2014. Source


Yu S.,Chongqing Medical University | Zhao J.,Chongqing Medical University | Wang X.,Chongqing Medical University | Lei S.,Jiangjin Center Hospital | And 4 more authors.
Neurochemical Research | Year: 2013

An herb-derived phenolic compound, 4-hydroxybenzyl alcohol (4-HBA), exhibits beneficial effects in cerebral ischemic injury. However, the molecular mechanisms underlying this observation remain unclear. Here we used an in vitro ischemic model of oxygen-glucose deprivation followed by reperfusion (OGD/R) and an in vivo ischemic model of middle cerebral artery occlusion to investigate the relevant neuroprotective mechanisms. We demonstrated that 4-HBA reduced the neuronal injury, LDH release, and up-regulation of 8-hydroxydeoxyguanosine (8-OHdG) induced by OGD/R. Furthermore, 4-HBA reduced the cerebral infarct size and improved the behavioral parameters after cerebral ischemia. These neuroprotective effects may be conferred by the 4-HBA mediated upregulation of the transcription factor nuclear factor E2-related factor 2 (Nrf2), peroxiredoxin 6 (Prdx6) and protein disulfide isomerase (PDI) by the use of 4-HBA. Interestingly, LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor, blocked the increase in phosphorylation of Akt and abolished the neuroprotection associated with 4-HBA. Our results suggested that 4-HBA protects neurons against cerebral ischemic injury, and this neuroprotection may occur through upregulation of Nrf2, Prdx6, and PDI expression via the PI3K/Akt pathway. © 2013 Springer Science+Business Media New York. Source


Yu S.-S.,Chongqing Medical University | Zhao J.,Chongqing Medical University | Lei S.-P.,Jiangjin Center Hospital | Lin X.-M.,Chongqing Medical University | And 2 more authors.
Neurochemical Research | Year: 2011

4-hydroxybenzyl alcohol (4-HBA), one of the phenolic constituents found in many herbal medicinal plants, exhibits beneficial effects in neurological disorders. In the present study, we evaluated 4-HBA's role in transient cerebral ischemia and its potential mechanism. Pre-treatment with 4-HBA (50,100 mg/kg) significantly reduced the cerebral infarct size and improved the neurological symptoms. Morphological examinations showed 4-HBA reduced the number of degenerated neurons. Oxidative stress was evaluated superoxide dismutase (SOD) activity and malondialdehyde (MDA) level. Anti-oxidative mechanisms were studied by Immunofluorescence staining and western immunoblot analysis. 4-HBA increased the expression of NAD(P)H: quinone oxidoreductase1 (NQO1) and ultimately inhibited oxidative stress. In addition, we evaluated the time course expression of NQO1, which was upregulated in the ischemic brain beginning at 1 h. Taken together, these results suggested that 4-HBA ameliorated cerebral injury in rats, This neuroprotective effect is likely related to its antioxidant activities. © 2010 Springer Science+Business Media, LLC. Source


Li Y.,Chongqing Medical University | Zhu J.,Chongqing Medical University | Liu Y.,Chongqing Medical University | Chen X.,Chongqing Medical University | And 6 more authors.
International Journal of Biological Sciences | Year: 2016

Abnormal activation of GSK-3β is associated with psychiatric and neurodegenerative disorders. However, no study has examined the effect of GSK-3β on cerebral ischemia/reperfusion injury. We used oxygen-glucose deprivation/reoxygenation (OGD/R) and middle cerebral artery occlusion (MCAO) as models of ischemia/reperfusion in rats in vitro and in vivo. Our study showed that knockdown of GSK-3β with a GSK-3β siRNA virus improved injury and increased viability of neurons subjected to OGD/R. Levels of total Nrf2, nuclear Nrf2, and Nrf2 downstream proteins sulfiredoxin (Srx1) and thioredoxin (Trx1) increased after transfection with the GSK-3β siRNA virus. GSK-3β siRNA increased SOD activity and decreased MDA levels. Overexpression of GSK-3β with a pcDNA-GSK-3β virus showed opposite results. We also demonstrated that intracerebroventricular injection of GSK-3β siRNA in rats ameliorated neurological deficits, reduced brain infarct volume and water content, and reduced damage to cerebral cortical neurons after MCAO. Changes in total Nrf2, nuclear Nrf2, Srx1, Trx1, SOD, and MDA were similar to those observed in vitro. Our results show for the first time that GSK-3β can influence cerebral ischemia/reperfusion injury. The effects may be due to regulating the Nrf2/ARE pathway and decreasing oxidative stress. These results suggest a potential new drug target for clinical treatment of stroke. © Ivyspring International Publisher. Source


Yu S.,Chongqing Medical University | Wang X.,Chongqing Medical University | Lei S.,Jiangjin Center Hospital | Chen X.,Chongqing Medical University | And 4 more authors.
Neurochemistry International | Year: 2015

Astrocytes appear to be important regulators of the inflammatory events that occur in stroke. Sulfiredoxin-1 (Srxn1), an endogenous antioxidant protein, exhibits neuroprotective effects. Although the mechanism by which Srxn1 negatively regulates oxidative and apoptotic pathways has been extensively characterized, the impact of Srxn1 on inflammation has not been well studied. In this study, we used oxygen-glucose deprivation followed by recovery (OGD/R) and hydrogen peroxide (H2O2) to mimic stress from cerebral ischemic damage on primary cultured astrocytes. We found that knockdown of Srxn1 by two shRNAs resulted in decreased cell viability of astrocytes. Decreased level of Srxn1 also correlated with excessive levels of proinflammatory cytokines and chemokines such as TNF-α, MPO, IL-1β, and IL-6. In addition, Srxn1 appeared to influence the strength of TLR4 signaling pathway; the expression of COX-2, IL-6, and NOS2 were strongly induced by OGD/R and H2O2 in astrocyte cultures with Srxn1-shRNAs. Our results suggested that loss of Srxn1 expression in astrocytes may cause excessive activation of inflammatory responses which contribute to OGD/R- and H2O2-induced cell death. Restoring Srxn1 function by gene therapy and/or pharmacology emerges as a promising strategy for the treatment of stroke and other chronic neurodegenerative diseases. © 2015 Elsevier Ltd. All rights reserved. Source

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