Publications by authors named "Zhengguo Qiu"

11 Publications

  • Page 1 of 1

Glutaredoxin 1 protects neurons from oxygen-glucose deprivation/reoxygenation (OGD/R)-induced apoptosis and oxidative stress via the modulation of GSK-3β/Nrf2 signaling.

J Bioenerg Biomembr 2021 May 6. Epub 2021 May 6.

Department of Anesthesiology, The First Hospital of Yulin, No. 93 Yuxi Street, Yulin, Shaanxi, 719000, China.

Increasing evidence has indicated that glutaredoxin 1 (GRX1) is a potent antioxidant protein that promotes cell survival under conditions of oxidative stress. Oxidative stress-induced neuronal injury contributes to cerebral ischemia/reperfusion injury. However, the role of GRX1-mediated antioxidant defense against neuronal damage during cerebral ischemia/reperfusion injury has not been thoroughly investigated. Thus, the objective of this study was to evaluate whether GRX1 protects neurons against oxygen-glucose deprivation/reoxygenation (OGD/R)-evoked oxidative stress injury in an in vitro model of cerebral ischemia/reperfusion injury. Our data revealed that GRX1 was induced by OGD/R treatment in neurons. Functional assays indicated that loss of GRX1 exacerbated OGD/R-induced apoptosis and the generation of reactive oxygen species (ROS), while GRX1 up-regulation protected against OGD/R-evoked neuronal injury. Further investigation revealed that GRX1 promoted the nuclear expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and enhanced transcription of the Nrf2/antioxidant response element (ARE) in GOD/R-exposed neurons. Furthermore, GRX1 promoted the activation of Nrf2/ARE associated with the modulation of glycogen synthase kinase-3β (GSK-3β). GSK-3β inhibition blocked GRX1 knockdown-mediated suppression of Nrf2 activation. Notably, the suppression of Nrf2 partially reversed GRX1-mediated anti-oxidative stress injury in OGD/R-exposed neurons. In summary, these findings indicate that GRX1 protects neurons against OGD/R-induced oxidative stress injury by enhancing Nrf2 activation via the modulation of GSK-3β. Our study suggests that GRX1 is a potential neuroprotective protein that protects against cerebral ischemia/reperfusion injury.
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http://dx.doi.org/10.1007/s10863-021-09898-0DOI Listing
May 2021

Alzheimer's Disease Determination by a Dual Probe on Gold Nanourchins and Nanohorn Hybrids.

Int J Nanomedicine 2021 19;16:2311-2322. Epub 2021 Mar 19.

Department of Surgery and Anesthesiology, Xi'an Hospital of Traditional Chinese Medicine, Xi'an, Shaanxi, People's Republic of China.

Background: Alzheimer's disease (AD) is a neurodegenerative chronic disorder that causes dementia and problems in thinking, cognitive impairment and behavioral changes. Amyloid-beta (Aβ) is a peptide involved in AD progression, and a high level of Aβ is highly correlated with severe AD. Identifying and quantifying Aβ levels helps in the early treatment of AD and reduces the factors associated with AD.

Materials And Methods: This research introduced a dual probe detection system involving aptamers and antibodies to identify Aβ. Aptamers and antibodies were attached to the gold (Au) urchin and hybrid on the carbon nanohorn-modified surface. The nanohorn was immobilized on the sensor surface by using an amine linker, and then a Au urchin dual probe was immobilized.

Results: This dual probe-modified surface enhanced the current flow during Aβ detection compared with the surface with antibody as the probe. This dual probe interacted with higher numbers of Aβ peptides and reached the detection limit at 10 fM with R=0.992. Furthermore, control experiments with nonimmune antibodies, complementary aptamer sequences and control proteins did not display the current responses, indicating the specific detection of Aβ.

Conclusion: Aβ-spiked artificial cerebrospinal fluid showed a similar response to current changes, confirming the selective identification of Aβ.
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http://dx.doi.org/10.2147/IJN.S302396DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7989959PMC
April 2021

Tectorigenin attenuates the OGD/R-induced HT-22 cell damage through regulation of the PI3K/AKT and the PPARγ/NF-κB pathways.

Hum Exp Toxicol 2021 Feb 16:960327121993213. Epub 2021 Feb 16.

Department of Anesthesiology, Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine, Xianyang, China.

Tectorigenin (TEC) is an effective compound that derived from many plants, such as . Evidence suggested that TEC has anti-tumor, anti-oxidant activity, anti-bacterial and anti-inflammatory effects. In addition, there has some evidence indicated that TEC is a potential anti-stroke compound; however, its specific roles and associated mechanism have not yet been elucidated. In the present study, we aimed to investigate the anti-inflammatory, anti-oxidant activity and anti-apoptosis effects of TEC on oxygen-glucose deprivation/reperfusion (OGD/R)-induced HT-22 cells, and clarified the relevant mechanisms. Here, we observed that TEC significantly promoted cell survival, impeded cell apoptosis, inhibited ROS and inflammatory cytokines IL-1β, IL-6, TNF-α production in OGD/R-induced HT-22 cells. Moreover, TEC activated PI3K/AKT signal pathway, increased PPARγ expression and inhibited NF-κB pathway activation in OGD/R-induced HT-22 cells. Further studies indicated that PPARγ inhibitor GW9662 activated NF-κB pathway after TEC treatment in OGD/R-induced HT-22 cells. Also, PI3K/AKT inhibitor LY294002, PPARγ inhibitor GW9662 and NF-κB activator LPS both reversed the effects of TEC on OGD/R-induced HT-22 cell biology. Taken together, this research confirmed that TEC benefit to HT-22 cell survival and against OGD/R damage through the PI3K/AKT and PPARγ/NF-κB pathways. These results indicated that TEC might be an effective compound in the treatment for ischemic brain injury.
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http://dx.doi.org/10.1177/0960327121993213DOI Listing
February 2021

17β-Estradiol Protects Neural Stem/Progenitor Cells Against Ketamine-Induced Injury Through Estrogen Receptor β Pathway.

Front Neurosci 2020 30;14:576813. Epub 2020 Sep 30.

Department of Anesthesiology, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, China.

Ketamine inhibits neural stem/progenitor cell (NSPC) proliferation and disrupts normal neurogenesis in the developing brain. 17β-Estradiol alleviates neurogenesis damage and enhances behavioral performance after ketamine administration. However, the receptor pathway of 17β-estradiol that protects NSPCs from ketamine-induced injury remains unknown. In the present study, we investigated the role of estrogen receptor α (ER-α) and estrogen receptor β (ER-β) in 17β-estradiol's protection against ketamine-exposed NSPCs and explored its potential mechanism. The primary cultured NSPCs were identified by immunofluorescence and then treated with ketamine and varying doses of ER-α agonist 4,4',4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (PPT) or ER-β agonist 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN) for 24 h. NSPC proliferation was analyzed by 5-bromo-2-deoxyuridine incorporation test. The expression of phosphorylated glycogen synthase kinase-3β (p-GSK-3β) was quantified by western blotting. It was found that treatment with different concentrations of PPT did not alter the inhibition of ketamine on NSPC proliferation. However, treatment with DPN attenuated the inhibition of ketamine on NSPC proliferation at 24 h after their exposure ( < 0.05). Furthermore, treatment with DPN increased p-GSK-3β expression in NSPCs exposed to ketamine. These findings indicated that ER-β mediates probably the protective effects of 17β-estradiol on ketamine-damaged NSPC proliferation and GSK-3β is involved in this process.
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http://dx.doi.org/10.3389/fnins.2020.576813DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7556164PMC
September 2020

Senescence marker protein 30 confers neuroprotection in oxygen-glucose deprivation/reoxygenation-injured neurons through modulation of Keap1/Nrf2 signaling: Role of SMP30 in OGD/R-induced neuronal injury.

Hum Exp Toxicol 2021 Mar 10;40(3):472-482. Epub 2020 Sep 10.

Department of Anesthesiology, The Second Affiliated Hospital of Xi'an Medical University, Xi'an, Shaanxi, China.

Senescence marker protein 30 (SMP30) is a senescence marker molecule and identified as a calcium regulatory protein. Currently, SMP30 has emerged as a cytoprotective protein in a wide range of cell types. However, the role of SMP30 in regulating neuronal survival during cerebral ischemia/reperfusion injury remains unclear. In the present study, we aimed to investigate the biological function and regulatory mechanism of SMP30 on neuronal survival using a cellular model induced by oxygen-glucose deprivation/reoxygenation (OGD/R). The results showed that SMP30 expression was significantly decreased by OGD/R exposure in neurons. Functional experiments demonstrated that SMP30 overexpression significantly rescued the decreased cell viability and attenuated the apoptosis and reactive oxygen species generation in OGD/R-exposed neurons. By contrast, SMP30 knockdown exhibited the opposite effect. Mechanism research revealed that SMP30 overexpression contributed to the activation of nuclear factor erythroid 2-related factor (Nrf2)/antioxidant response element (ARE) signaling associated with downregulation of Kelch-like ECH-associated protein (Keap1). Keap1 overexpression or Nrf2 silencing significantly reversed SMP30-mediated neuroprotection against OGD/R-induced injury. Overall, these findings demonstrate that SMP30 overexpression protects neurons from OGD/R-induced apoptosis and oxidative stress by enhancing Nrf2/ARE antioxidant signaling via inhibition of Keap1. These data highlight the importance of the SMP30/Keap1/Nrf2/ARE signaling axis in regulating neuronal survival during cerebral ischemia/reperfusion injury.
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http://dx.doi.org/10.1177/0960327120954243DOI Listing
March 2021

Attenuation of Acute Intracerebral Hemorrhage-Induced Microglial Activation and Neuronal Death Mediated by the Blockade of Metabotropic Glutamate Receptor 5 In Vivo.

Neurochem Res 2020 May 5;45(5):1230-1243. Epub 2020 Mar 5.

Institute of Neurobiology, Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, Xi'an, 710061, Shaanxi, People's Republic of China.

The activation of microglia in response to intracerebral hemorrhagic stroke is one of the principal components of the progression of this disease. It results in the formation of pro-inflammatory cytokines that lead to neuronal death, a structural deterioration that, in turn interferes with functional recovery. Metabotropic glutamate receptor 5 (mGluR5) is highly expressed in reactive microglia and is involved in the pathological processes of brain disorders, but its role in intracerebral hemorrhage (ICH) remains unknown. We hypothesized that mGluR5 regulates microglial activation and ICH maintenance. In this study, collagenase-induced ICH mice received a single intraperitoneal injection of the mGluR5 antagonist-, MTEP, or vehicle 2 h after injury. We found that acute ICH upregulated mGluR5 and microglial activation. mGluR5 was highly localized in reactive microglia in the peri-hematomal cortex and striatum on days 3 and 7 post-ICH. The MTEP-mediated pharmacological inhibition of mGluR5 in vivo resulted in the substantial attenuation of acute microglial activation and IL-6, and TNF-α release. We also showed that the blockade of mGluR5 markedly reduced cell apoptosis, and neurodegeneration and markedly elevated neuroprotection. Furthermore, the MTEP-mediated inhibition of mGluR5 significantly reduced the lesion volume and improved functional recovery. Taken together, our results demonstrate that ICH injury enhances mGluR5 expression in the acute and subacute stages and that mGluR5 is highly localized in reactive microglia. The blockade of mGluR5 reduces ICH-induced acute microglial activation, provides neuroprotection and promotes neurofunctional recovery after ICH. The inhibition of mGluR5 may be a relevant therapeutic target for intracerebral hemorrhagic stroke.
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http://dx.doi.org/10.1007/s11064-020-03006-1DOI Listing
May 2020

Dexmedetomidine Alleviates Neurogenesis Damage Following Neonatal Midazolam Exposure in Rats through JNK and P38 MAPK Pathways.

ACS Chem Neurosci 2020 02 10;11(4):579-591. Epub 2020 Feb 10.

Department of Anesthesiology , The Second Affiliated Hospital of Xi'an Jiaotong University , Xi'an 710004 , China.

Midazolam, a widely used anesthetic, inhibits proliferation of neural stem cells (NSCs) and induces neuroapoptosis in neonates. Dexmedetomidine, an effective auxiliary medicine in clinical anesthesia, protects the developing brain against volatile anesthetic-induced neuroapoptosis. Whether dexmedetomidine protects against neurogenesis damage induced by midazolam remains unknown. This study aims to clarify the protective effect of dexmedetomidine on midazolam-induced neurogenesis damage and explore its potential mechanism. Postnatal 7-day-old Sprague-Dawley (SD) rats and cultured NSCs were treated with either normal saline, midazolam, or dexmedetomidine combined with midazolam. The rats were sacrificed at 1, 3, and 7 days after treatment. Cell proliferation was assessed by 5-bromodeoxyurdine (BrdU) incorporation. Cell viability was determined using MTT assay. Cell differentiation and apoptosis were detected by immunofluorescent staining and terminal dUTP nick-end labeling (TUNEL), respectively. The protein levels of p-JNK, p-P38, and cleaved caspase-3 were quantified using Western blotting. Midazolam decreased cell proliferation and increased cell apoptosis in the subventricular zone (SVZ), the subgranular zone (SGZ) of the hippocampus, and cultured NSCs. Moreover, midazolam decreased cell viability and increased the expression of p-JNK and p-P38 in cultured NSCs. Co-treatment with dexmedetomidine attenuated midazolam-induced changes in cell proliferation, viability, apoptosis, and protein expression of p-JNK and p-P38 in cultured NSCs. Midazolam and dexmedetomidine did not affect the differentiation of the cultured NSCs. These results indicate that dexmedetomidine alleviated midazolam-induced neurogenesis damage via JNK and P38 MAPK pathways.
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http://dx.doi.org/10.1021/acschemneuro.9b00611DOI Listing
February 2020

Trigonelline protects hippocampal neurons from oxygen-glucose deprivation-induced injury through activating the PI3K/Akt pathway.

Chem Biol Interact 2020 Feb 11;317:108946. Epub 2020 Jan 11.

Department of Neurology, The Hospital of Xidian Group, Xi'an, Shaanxi, 710077, China. Electronic address:

Trigonelline is a plant alkaloid that has generated interest for its neuroprotective roles in brain pathology. However, the protective effect of trigonelline on cerebral ischemia/reperfusion (I/R) injury and the potential mechanism have not been fully evaluated. Our results showed that trigonelline pretreatment ameliorated oxygen-glucose deprivation/reperfusion (OGD/R)-induced hippocampal neurons injury. The OGD/R-caused reactive oxygen species (ROS) generation and decreased concentrations of superoxide dismutases (SOD) and glutathione peroxidase (GPx) were markedly attenuated by trigonelline. In addition, the increased levels of TNF-α, IL-6 and IL-1β in OGD/R-induced hippocampal neurons were significantly decreased by trigonelline pretreatment. Trigonelline also suppressed caspase-3 activity and bax expression, and induced bcl-2 expression in OGD/R-induced hippocampal neurons. Furthermore, trigonelline induced the activation of PI3K/Akt pathway in hippocampal neurons exposed to OGD/R condition. Inhibition of PI3K/Akt signaling reversed the protective effects of trigonelline on OGD/R-induced hippocampal neurons injury. Taken together, these findings indicated that trigonelline protected hippocampal neurons from OGD/R-induced injury, which was mediated by the activation of PI3K/Akt signaling pathway.
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http://dx.doi.org/10.1016/j.cbi.2020.108946DOI Listing
February 2020

Dexmedetomidine Inhibits Neuroinflammation by Altering Microglial M1/M2 Polarization Through MAPK/ERK Pathway.

Neurochem Res 2020 Feb 10;45(2):345-353. Epub 2019 Dec 10.

Department of Anesthesiology, The Second Affiliated Hospital of Xi'an Jiaotong University, 157# West 5 Road, Xi'an, 710004, Shaanxi, China.

Neuroinflammation is critical in the pathogenesis of neurological diseases. Microglial pro-inflammatory (M1) and anti-inflammatory (M2) status determines the outcome of neuroinflammation. Dexmedetomidine exerts anti-inflammatory effects in many neurological conditions. Whether dexmedetomidine functions via modulation of microglia M1/M2 polarization remains to be fully elucidated. In the present study, we investigated the anti-inflammatory effects of dexmedetomidine on the neuroinflammatory cell model and explored the potential mechanism. BV2 cells were stimulated with LPS to establish a neuroinflammatory model. The cell viability was determined with MTT assay. NO levels were assessed using a NO detection kit. The protein levels of IL-10, TNF-α, iNOS, CD206, ERK1/2, and pERK1/2 were quantified using Western blotting. LPS significantly increased pro-inflammatory factors TNF-α and NO, and M1 phenotypic marker iNOS, and decreased anti-inflammatory factor IL-10 and M2 phenotypic marker CD206 in BV2 cells. Furthermore, exposure of BV2 cells to LPS significantly raised pERK1/2 expression. Pretreatment with dexmedetomidine attenuated LPS-elicited changes in p-ERK, iNOS, TNF-α, NO, CD206 and IL-10 levels in BV2 cells. However, co-treatment with dexmedetomidine and LM22B-10, an agonist of ERK, reversed dexmedetomidine-elicited changes in p-ERK, iNOS, TNF-α, NO, CD206 and IL-10 levels in LPS-exposed BV2 cells. We, for the first time, showed that dexmedetomidine increases microglial M2 polarization by inhibiting phosphorylation of ERK1/2, by which it exerts anti-inflammatory effects in BV2 cells.
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http://dx.doi.org/10.1007/s11064-019-02922-1DOI Listing
February 2020

Edaravone protects primary-cultured rat cortical neurons from ketamine-induced apoptosis via reducing oxidative stress and activating PI3K/Akt signal pathway.

Mol Cell Neurosci 2019 10 7;100:103399. Epub 2019 Sep 7.

Department of Anesthesiology, The Second Affiliated Hospital, Xi'an Jiaotong University, 157# West 5 road, Xi'an, Shaanxi 710004, China. Electronic address:

Ketamine caused neuroapoptosis in the development of rat brain, in which oxidative stress play an important role. Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a free radical scavenger, exerts neuroprotective effects in many neurological disease models. Here we investigated whether edaravone protects primary-cultured neurons against ketamine-induced apoptosis and its potential mechanism. Edaravone increased neuronal viability, decreased neuronal apoptosis, increased the ratio of Bcl-2/Bax after ketamine exposure. Edaravone also increased superoxide dismutase (SOD) activity and decreased malondialdehyde (MDA) level in ketamine-exposed neurons. In addition, edaravone increased protein levels of phosphorylated-protein kinase B (p-Akt), phosphorylated-glycogen synthase kinase-3β (p-GSK-3β) and phosphorylated-forkhead box protein O1 (p-FoxO1) in ketamine-exposed neurons. The neuroprotective effects of edaravone were reversed by LY294002, a specific phosphatidylinositol 3-kinase (PI3K) inhibitor. These findings demonstrated that edaravone protected neurons against ketamine-induced apoptosis by diminishing oxidative stress and activating PI3K/Akt signal pathway.
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http://dx.doi.org/10.1016/j.mcn.2019.103399DOI Listing
October 2019

Overexpression of TRIM26 suppresses the proliferation, metastasis, and glycolysis in papillary thyroid carcinoma cells.

J Cell Physiol 2019 08 29;234(10):19019-19027. Epub 2019 Mar 29.

Department of Tumor Radiotherapy, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

Papillary thyroid carcinoma (PTC) is the common subtype of thyroid cancer, which is a common endocrine malignancy. Tripartite motif 26 (TRIM26) has been found to act as a tumor suppressor in several cancers. However, the functional roles of TRIM26 in PTC remain unknown. In this study, we examined the TRIM26 expression in PTC and evaluated the effects of TRIM26 on proliferation, metastasis, and glycolysis in PTC cells. The results proved that TRIM26 was significantly downregulated in PTC tissues and cell lines. TRIM26 overexpression inhibited cell proliferation, migration, and invasion in PTC cells. TRIM26 overexpression also suppressed the epithelial-to-mesenchymal transition process. Besides, overexpression of TRIM26 caused significant decrease in glucose uptake and lactate production in PTC cells. Further investigations revealed that TRIM26 overexpression inhibited the activation of PI3K/Akt pathway. Treatment with an activator (740Y-P) of the PI3K/AKT pathway reversed the antitumor effects of TRIM26 on PTC cells. These findings provided evidence that TRIM26 acted as a tumor suppressor in PTC.
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http://dx.doi.org/10.1002/jcp.28541DOI Listing
August 2019