Chunxia Luo

Third Military Medical University, Ch’ung-ch’ing-shih, Chongqing Shi, China

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Publications (16)36.72 Total impact

  • Yujie Chen · Chunxia Luo · Mingyue Zhao · Qiang Li · Rong Hu · John H Zhang · Zhi Liu · Hua Feng ·
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    ABSTRACT: The aim of this study was to investigate whether the phosphatase and tensin homolog deleted on chromosome ten (PTEN) inhibitor dipotassium bisperoxo(pyridine-2-carboxyl) oxovanadate (BPV(pic)) attenuates early brain injury by modulating α-amino-3-hydroxy-5-methyl-4-isoxa-zolep-propionate (AMPA) receptor subunits after subarachnoid hemorrhage (SAH). A standard intravascular perforation model was used to produce the experimental SAH in Sprague-Dawley rats. BPV(pic) treatment (0.2mg/kg) was evaluated for effects on neurological score, brain water content, Evans blue extravasation, hippocampal neuronal death and AMPA receptor subunits alterations after SAH. We found that BPV(pic) is effective in attenuating BBB disruption, lowering edema, reducing hippocampal neural death and improving neurological outcomes. In addition, the AMPA receptor subunit GluR1 protein expression at cytomembrane was downregulated, whereas the expression of GluR2 and GluR3 was upregulated after BPV(pic) treatment. Our results suggest that PTEN inhibited by BPV(pic) plays a neuroprotective role in SAH pathophysiology, possibly by alterations in glutamate AMPA receptor subunits. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    Neuroscience Letters 01/2015; 588. DOI:10.1016/j.neulet.2015.01.005 · 2.03 Impact Factor
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    ABSTRACT: Norrin and its receptor Frizzled-4 have important roles in the blood-brain barrier development. This study is to investigate a potential role and mechanism of Norrin/Frizzled-4 on protecting blood-brain barrier integrity after subarachnoid hemorrhage (SAH). One hundred and seventy-eight male Sprague-Dawley rats were used. SAH model was induced by endovascular perforation. Frizzled-4 small interfering RNA was injected intracerebroventricularly 48 hours before SAH. Norrin was administrated intracerebroventricularly 3 hours after SAH. SAH grade, neurological scores, brain water content, Evans blue extravasation, western blots, and immunofluorescence were used to study the mechanisms of Norrin and its receptor regulation protein TSPAN12, as well as neurological outcome. Endogenous Norrin and TSPAN12 expression were increased after SAH, and Norrin was colocalized with astrocytes marker glial fibrillary acidic protein in cortex. Exogenous Norrin treatment significantly alleviated neurobehavioral dysfunction, reduced brain water content and Evans blue extravasation, promoted β-catenin nuclear translocation, and increased Occludin, VE-Cadherin, and ZO-1 expressions. These effects were abolished by Frizzled-4 small interfering RNA pretreated before SAH. Norrin protected blood-brain barrier integrity and improved neurological outcome after SAH, and the action of Norrin appeared mediated by Frizzled-4 receptor activation, which promoted β-catenin nuclear translocation, which then enhanced Occludin, VE-Cadherin, and ZO-1 expression. Norrin might have potential to protect blood-brain barrier after SAH. © 2014 American Heart Association, Inc.
    Stroke 12/2014; 46(2). DOI:10.1161/STROKEAHA.114.007265 · 5.72 Impact Factor
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    ABSTRACT: Previous neuroimaging studies have revealed that both gray matter (GM) and white matter (WM) are altered in several morphological aspects in amyotrophic lateral sclerosis (ALS). However, the relations between GM and WM measures and their contributions to clinical features remain in doubt. In this study, we acquired high-resolution diffusion tensor imaging along with structural magnetic resonance imaging data on 20 patients with clinical evidence of ALS and 21 matched healthy controls. WM microstructural metrics and cortical thickness were measured to characterize the whole brain WM and GM degenerative patterns. Probabilistic diffusion tractography was used to reconstruct the tracts from the WM regions characterized by fractional anisotropy (FA) decrease in patients. Decreased FA and increased radial diffusivity was observed in WM regions of the bilateral corticospinal tracts (CST) and callosal motor fibers in the ALS patients, while the superior longitudinal fasciculus exhibited a changing trend. Cortical thinning was found in the anatomically congruent regions, including the motor-related cortices (i.e., bilateral precentral gyri, dorsal premotor cortices, and left supplementary motor area), prefrontal and occipito-parietal regions. However, there was no significant relationship between FA reduction and cortical thinning. Finally, patients with faster clinical progression showed more severe cortical thinning of the left precentral gyrus and FA reduction of the left CST. Together, these findings suggest that ALS is multisystem degeneration involving both the widespread cortices and the underlying WM fibers. GM and WM changes might play distinct roles in the disease progression.
    Journal of Neurology 01/2014; 261(2):412-421. DOI:10.1007/s00415-013-7215-5 · 3.38 Impact Factor
  • Yunfeng Yang · Chunxia Luo · Hongping Miao · Zhi Chen ·
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    ABSTRACT: Thrombolysis with recombinant tissue plasminogen activator (rt-PA) is clinically effective at treating acute ischemic stroke. However, the use of thrombolytic therapy is associated with an increased risk of symptomatic intracerebral hemorrhage (sICH). Whether unacceptable surgical hemorrhage occurs after emergent decompressive craniotomy during the first hours for sICH remains unknown. We report a 69-year-old Chinese woman with a fibrinolysis-related sICH, and discuss the efficacy and the safety of craniotomy in this setting. An urgent decompressive craniotomy was performed through a standard pterional approach without any procoagulant therapy before operation. No unacceptable surgical hemorrhage occurred during the first hours after onset of sICH, and the outcome of this patient is fairly good. Early urgent decompressive craniectomy in the treatment of fibrinolysis-related sICH may be a safe therapy, which may improve clinical outcomes.
    Neurosciences 10/2012; 17(4):368-70. · 0.71 Impact Factor
  • Zhi Chen · Yunfeng Yang · Hongpin Miao · Jingyu Chen · Chunxia Luo · Hua Feng · Gang Zhu ·
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    ABSTRACT: To assess the feasibility and result of endovascular treatments for ruptured peripheral intracranial aneurysms. We retrospectively reviewed our experience and results of endovascular treatments for a series of 18 consecutive patients with ruptured distal intracranial aneurysms at the Department of Neurosurgery, Southwest Hospital, Chongqing, China between January 2005 and June 2010. Depending on the location and shape of the aneurysms, we used various therapeutic strategies including selective aneurysmal coiling, parent artery (and aneurysm) occlusion, stent-assisted coiling, and microcatheter-assisted coiling. Endovascular embolization was technically successful in all patients. Five patients were treated by selective aneurysm coiling; 5 patients were embolized with the stent-assisted technique or microcatheter-assisted technique. In the remaining 8 patients, the parent arteries, or together with the aneurysms were occluded using coils or glue. No procedure complication such as thrombosis or aneurysmal rupture was encountered during treatment. Two patients treated with parent artery occlusion developed acute or delayed transient ischemic symptoms, but they eventually made a good recovery. No patient has experienced postprocedural hemorrhage during the follow-up period (5-66 months; mean, 22.2 months). Endovascular treatment is a feasible and effective therapeutic alternative for peripheral intracranial aneurysms.
    Neurosciences 04/2012; 17(2):133-8. · 0.71 Impact Factor
  • Bo Li · Chunxia Luo · Weihua Tang · Zhi Chen · Qiang Li · Bo Hu · Jiangkai Lin · Gang Zhu · John H Zhang · Hua Feng ·
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    ABSTRACT: Disruption of ionic homeostasis and neuronal hyperexcitability contribute to early brain injury after subarachnoid hemorrhage (SAH). The hyperpolarization-activated/cyclic nucleotide (HCN)-gated channels play critical role in the regulation of neuronal excitability in hippocampus CA1 region and neocortex, in which the abnormal neuronal activities are more readily provoked. This study was to investigate the interactions between HCN channels and hyperneuronal activity after experimental SAH. The present results from whole-cell recordings in rat brain slices indicated that (1) perfusion of hemoglobin (Hb)-containing artificial CSF produced neuronal hyperexcitability and inhibited HCN currents in CA1 pyramidal neurons, (2) nitric oxide/Spermine (NO/Sp), a controlled releaser of nitric oxide, attenuated neuronal excitability and enhanced HCN currents in CA1 pyramidal neurons, while L-nitroarginine (L-NNA), an inhibitor of nitric oxide synthase, reduced the HCN currents; and (3) the inhibitory action of Hb on HCN currents was reversed by application of NO/Sp, which also reduced neuronal hyperexcitability; conversely, L-NNA enhanced inhibitory action of Hb on HCN currents. Additionally, Hb perfusion scavenged the production of nitric oxide and decreased the expression of HCN1 subunits in CA1 region. In the rat SAH model, the expression of HCN1, both at mRNA and protein level, decreased in hippocampus CA1 region at 24 h and more pronounced at 72 h after SAH. These observations demonstrated a reduction of HCN channels expression after SAH and Hb reduced HCN currents in hippocampus CA1 pyramidal neurons. Inhibition of HCN channels by Hb may be a novel pathway for inducing the hyperneuronal excitability after SAH.
    The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 02/2012; 32(9):3164-75. DOI:10.1523/JNEUROSCI.5143-11.2012 · 6.34 Impact Factor
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    ABSTRACT: Traumatic brain injury (TBI) is a major health problem all over the world. It frequently causes a considerable social burden because of its high incidence of death and long-term disability, especially in the case of severe TBI. Recent studies revealed that the spleen might contribute to secondary brain injury after ischemia or intracerebral hemorrhage. The purpose of this study was to evaluate the significance of the spleen in traumatic brain edema after severe TBI. We established a severe TBI model with rats and performed splenectomy to observe the mortality, brain water content, cognitive function (water maze), and cytokines levels, including interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), IL-6, and IL-10, in the blood plasma (enzyme-linked immunosorbent assay) and their mRNA expression levels in injured brain tissue (quantitative reverse transcriptase-polymerase chain reaction). The immediate splenectomy after TBI significantly decreased the death rate from 35.42% to 14.89% and eliminated the brain water content of the injured brain, especially at days 2 and 3. The Morris water maze assessment showed an improved spatial reference memory in rats that underwent both TBI and splenectomy when compared with those in the TBI group, 4 weeks later. Splenectomy reduced the IL-1β, TNF-α, and IL-6 contents in the blood serum after TBI, and the mRNA expression levels of IL-1β, TNF-α, and IL-6 in the ipsilateral brain tissue also decreased. Our study demonstrates that splenectomy has a protective effect on rats with severe TBI by inhibiting proinflammatory cytokines, including IL-1β, TNF-α, and IL-6, both systematically and locally in the injured brain, hence leading to a decreased mortality and improved cognitive function.
    The Journal of trauma 07/2011; 71(1):141-7. DOI:10.1097/TA.0b013e3181f30fc9 · 2.96 Impact Factor
  • Jun Hu · Wei Chen · Yaguang Wu · Kangning Chen · Chunxia Luo · Yong Liang · Shugui Shi ·

    Neurology India 05/2011; 59(3):474-5. DOI:10.4103/0028-3886.82749 · 1.23 Impact Factor
  • Chunxia Luo · Bin Yi · Wenhui Fan · Kangning Chen · Li Gui · Zhi Chen · Lusi Li · Hua Feng · Luxiang Chi ·
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    ABSTRACT: We reported previously that ecdysterone (EDS) improves neurologic function after experimental stroke. However, the underlying mechanism remained unclear. The present study was conducted to test whether ecdysterone improves neurologic function by enhancing astrocyte activation and angiogenesis after focal cerebral ischemia in rats. Focal cerebral ischemia model was conducted by middle cerebral artery occlusion (MCAO). EDS was intraperitoneally injected at 20 mg kg1 daily for 7 days after MCAO. Neurologic recovery was assessed using the neurologic severity scores. Microvessel density and GFAP expression were detected with immunostaining and analyzed quantitatively with image system. Treatment with EDS significantly improved functional recovery, along with increases in density of cerebral microvessels and astrocyte activation. Microvessel density was significantly higher in EDS treated group than in ischemia control group at all time points, and reached a peak on day 14. EDS treated group had substantial increment in GFAP immunoreactive cells, darker staining color, more and longer nerve processes, higher GFAP expression and area of immunoreactive cells at each time point. Our data suggest that EDS treatment enhanced angiogenesis and astrocyte activation which could contribute to functional recovery.
    Acta neurochirurgica. Supplement 01/2011; 110(Pt 1):151-5. DOI:10.1007/978-3-7091-0353-1_26
  • Chunxia Luo · Bin Yi · Zhi Chen · Weihua Tang · Yujie Chen · Rong Hu · Zhi Liu · Hua Feng · John H Zhang ·
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    ABSTRACT: The purpose of the present study was to observe the proliferation of cerebral arterial smooth muscle cell (CASMC) induced by oxyhemoglobin (Oxyhb) and interfered by Adenovirus-mediate-PKGI (Ad-PKGI), and to investigate the potential regulative role of the PKGI gene in the molecule mechanism of cerebral vasospasm (CVS) after Subarachnoid hemorrhage (SAH). Tissue-sticking method was used for primary cultured rat CASMCs. Semi-quantitative reverse transcription and polymerase chain reaction (RT-PCR) and western blot were used to examine the PKGI mRNA and protein expressions after CASMC were transfected by Ad-PKG. The proliferation of CASMCs was determined by MTT assay and 3H-TdR incorporation. Ad-PKGI could be transfected into CASMCS and highly express. Oxyhemoglobin could stimulate the proliferation of CASMC; the value of 3H-TdR incorporation and the absorbance value of MTT increased and could block up after CASMC was transfected by Ad-PKG. The results suggested that the PKG signaling pathway might play an important role in CVS after SAH, and the PKG gene might be a target point of gene therapy.
    Acta neurochirurgica. Supplement 01/2011; 110(Pt 1):167-71. DOI:10.1007/978-3-7091-0353-1_29
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    ABSTRACT: The relationship between cancer-initiating cells and cancer-related inflammation is unclear. Exploring the interaction between glioma-initiating cells (GICs) and tumor-associated microglia/macrophages (TAM/Ms) may offer us an opportunity to further understand the inflammatory response in glioma and the cellular/molecular features of the GIC niche. Here,we reported a positive correlation between the infiltration of TAM/Ms and the density of GICs. The capacity of GICs to recruit TAM/Ms was stronger than that of adhesive glioma cells (AGCs) in vitro. In vivo experiments suggested that implantations formed by GICs had a higher level of TAM/M infiltration than those formed by AGCs. Our studies indicate a predominant role of GICs in microglia/macrophages tropism to glioma and a close positive correlation between the distribution of GICs and TAM/Ms. As an important part of cancer-related inflammation, TAM/Ms may participate in the architecture of the GIC niche.
    Journal of neuroimmunology 11/2010; 232(1-2):75-82. DOI:10.1016/j.jneuroim.2010.10.011 · 2.47 Impact Factor
  • Chunxia Luo · Bin Yi · Guocai Tao · Mei Li · Zhi Chen · Weihua Tang · John H Zhang · Hua Feng ·
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    ABSTRACT: Inflammation plays an important role in the pathogenesis of early brain injury after subarachnoid haemorrhage. Adenosine A3 receptor (A3R) activation produces anti-inflammatory effects. In this study, the effects of a selective A3R agonist, 2-chloro-N⁶-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (CL-IB-MECA), on early brain injury and inflammatory response after subarachnoid haemorrhage were studied. Our results showed that mortality, neurological impairment and brain oedema were significantly attenuated after the administration of CL-IB-MECA. Moreover, treatment with CL-IB-MECA inhibited microglial activation and reduced the expression of proinflammatory cytokines including tumour necrosis factor-α and interleukin-1β. These data suggest that activation of A3R provides a neuroprotective effect against brain injury after subarachnoid haemorrhage, and that these effects may be associated with the anti-inflammatory properties of A3R.
    Neuroreport 09/2010; 21(13):892-6. DOI:10.1097/WNR.0b013e32833dbd13 · 1.52 Impact Factor
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    ABSTRACT: A glial scar is thought to be responsible for halting neuroregeneration following spinal cord injury (SCI). However, little quantitative evidence has been provided to show the relationship of a glial scar and axonal regrowth after injury. In this study performed in rats and dogs, a traumatic SCI model was made using a weight-drop injury device, and tissue sections were stained with H & E for immunohistochemical analysis. The function and behavior of model animals were tested using electrophysiological recording and the Basso-Beattie-Bresnahan Locomotor Rating Scale, respectively. The cavity in the spinal cord after SCI in dogs was observed using MR imaging. The morphological results showed that the formation of an astroglial scar was defined at 4 weeks after SCI. While regenerative axons reached the vicinity of the lesion site, the glial scar blocked the extension of regrown axons. In agreement with these findings, the electrophysiological, behavioral, and in vivo MR imaging tests showed that functional recovery reached a plateau at 4 weeks after SCI. The thickness of the glial scars in the injured rat spinal cords was also measured. The mean thickness of the glial scar rostral and caudal to the lesion cavity was 107.00 +/- 20.12 microm; laterally it was 69.92 +/- 15.12 microm. These results provide comprehensive evidence indicating that the formation of a glial scar inhibits axonal regeneration at 4 weeks after SCI. This study reveals a critical time window of postinjury recovery and a detailed spatial orientation of glial scar, which would provide an important basis for the development of therapeutic strategy for glial scar ablation.
    Journal of neurosurgery. Spine 08/2010; 13(2):169-80. DOI:10.3171/2010.3.SPINE09190 · 2.38 Impact Factor
  • Chunxia Luo · Bin Yi · Li Bai · Yongzhi Xia · Guansong Wang · Guisheng Qian · Hua Feng ·
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    ABSTRACT: Recent findings identify the role of proliferation of pulmonary artery smooth muscle cells (PASMCs) in pulmonary vascular remodeling. Phosphoinositide 3 kinase (PI3K) and serine/threonine kinase (Akt) proteins are expressed in vascular smooth muscle cells. In addition, phosphatase and tensin homolog deleted on chromosome 10 (PTEN) has been identified as a negative regulator of cytokine signaling that inhibits the PI3K-Akt pathway. However, little is known about the role of PTEN/Akt signaling in hypoxia-associated vascular remodeling. In this study, we found that hypoxia-induced the expression of Akt1 mRNA and phosphorylated protein by at least twofold in rat PASMCs. Phospho-PTEN significantly decreased in the nuclei of PASMCs after hypoxic stimulation. After forcing over-expression of PTEN by adenovirus-mediated PTEN (Ad-PTEN) transfection, the expression of phospho-Akt1 was significantly suppressed in PASMCs at all time-points measured. Additionally, we showed here that hypoxia increased proliferation of PASMCs by nearly twofold and over-expression of PTEN significantly inhibited hypoxia-induced PASMCs proliferation. These findings suggest that phospho-PTEN loss in the nuclei of PASMCs under hypoxic conditions may be the major cause of aberrant activation of Akt1 and may, therefore, play an important role in hypoxia-associated pulmonary arterial remodeling. Finally, the fact that transfection with Ad-PTEN inhibits the phosphorylation of Akt1 in PASMCs suggests a potential therapeutic effect on hypoxia-associated pulmonary arterial remodeling.
    Biochemical and Biophysical Research Communications 07/2010; 397(3):486-92. DOI:10.1016/j.bbrc.2010.05.140 · 2.30 Impact Factor
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    ABSTRACT: Brain-iron deposition has been proposed to play an important role in the pathophysiology of Parkinson's disease (PD). The aim of this study was to evaluate the feasibility of characterizing iron deposition in PD using susceptibility-weighted imaging (SWI), and to investigate the correlation of brain-iron accumulation with the clinical status in patients with PD. Forty patients with PD without dementia and 26 age- and sex-matched healthy controls underwent high-resolution susceptibility-weighted magnetic resonance (MR) imaging. The phase shift values of the bilateral red nucleus (RN), substantia nigra (SN), caudate nucleus (CA), globus pallidus (GP), putamen (PU), thalamus (TH) and frontal white matter (FWM) were examined for their relationship with the clinical status. The iron concentrations of the regions involved in PD, such as the SN, increased more significantly, while those in other regions of interest (ROI) did not elevate significantly. No correlation between the increase of the iron concentrations of the SN and duration of PD was observed. PD, however, was closely associated with the Unified Parkinson's Disease Rating Scale motor score (UPDRS-III). No significant differences were found between earlier-onset and later-onset PD patients in terms of the iron concentrations of the SN. Brain-iron concentration can be evaluated by SWI. Also, the brain-iron concentration in the SN correlated with UPDRS motor score, indicating that iron concentration can function as an in vivo biomarker to objectively evaluate the status of PD.
    Brain research 03/2010; 1330:124-30. DOI:10.1016/j.brainres.2010.03.036 · 2.84 Impact Factor
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    ABSTRACT: The purpose of the present study was to investigate the interactions between brain microvascular endothelial cells (BMEC) and mesenchymal stem cells (MSC) under hypoxic conditions. Primary cultured human bone marrow MSC and rat BMEC were isolated, cultured and identified. Vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) were detected in the conditioned media of BMEC and MSC under normal and hypoxic conditions using ELISA. MSC differentiation was analyzed using flow cytometry and fluorescence immunocytochemistry. Transendothelial electrical resistance (TEER) techniques were employed to measure changes in permeability across the BMEC monolayer. Under hypoxic conditions, the concentration of VEGF and MMP-9 in the conditioned media increased significantly, with greater levels in the MSC than the BMEC media. Primary MSC did not express vWF and Flk-1. MSC were co-cultured with BMEC under hypoxic conditions 5 days later. MSC expressing Flk-1 accounted for 23.64+/-2.50% (n=6, P<0.001) of the total number of cells. Interestingly, some Flk-1 positive cells began to coexpress vWF simultaneously. Under hypoxic conditions, MSC conditioned media significantly enhanced the proliferation and migration of BMEC. In addition, MSC decreased the TEER of the BMEC monolayer (lowest values: 50.5+/-2.6% of the original), which could partially be inhibited by both anti-VEGF antibody and MMP-9 inhibitor. These data indicate that under hypoxic conditions BMEC induce MSC to differentiate into endothelial cells, and MSC enhance the proliferation and migration of BMEC through paracrine functions, while simultaneously increasing the permeability of the BMEC monolayer.
    Microvascular Research 01/2008; 75(1):59-67. DOI:10.1016/j.mvr.2007.06.003 · 2.13 Impact Factor

Publication Stats

227 Citations
36.72 Total Impact Points


  • 2008-2015
    • Third Military Medical University
      • Department of Neurosurgery
      Ch’ung-ch’ing-shih, Chongqing Shi, China