Publications by authors named "L Jing"

1,467 Publications

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Exosomes derived from bone marrow mesenchymal stem cells protect the injured spinal cord by inhibiting pericyte pyroptosis.

Neural Regen Res 2022 Jan;17(1):194-202

Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.

Mesenchymal stem cell (MSC) transplantation is a promising treatment strategy for spinal cord injury, but immunological rejection and possible tumor formation limit its application. The therapeutic effects of MSCs mainly depend on their release of soluble paracrine factors. Exosomes are essential for the secretion of these paracrine effectors. Bone marrow mesenchymal stem cell-derived exosomes (BMSC-EXOs) can be substituted for BMSCs in cell transplantation. However, the underlying mechanisms remain unclear. In this study, a rat model of T10 spinal cord injury was established using the impact method. Then, 30 minutes and 1 day after spinal cord injury, the rats were administered 200 μL exosomes via the tail vein (200 μg/mL; approximately 1 × 10 BMSCs). Treatment with BMSC-EXOs greatly reduced neuronal cell death, improved myelin arrangement and reduced myelin loss, increased pericyte/endothelial cell coverage on the vascular wall, decreased blood-spinal cord barrier leakage, reduced caspase 1 expression, inhibited interleukin-1β release, and accelerated locomotor functional recovery in rats with spinal cord injury. In the cell culture experiment, pericytes were treated with interferon-γ and tumor necrosis factor-α. Then, Lipofectamine 3000 was used to deliver lipopolysaccharide into the cells, and the cells were co-incubated with adenosine triphosphate to simulate injury in vitro. Pre-treatment with BMSC-EXOs for 8 hours greatly reduced pericyte pyroptosis and increased pericyte survival rate. These findings suggest that BMSC-EXOs may protect pericytes by inhibiting pyroptosis and by improving blood-spinal cord barrier integrity, thereby promoting the survival of neurons and the extension of nerve fibers, and ultimately improving motor function in rats with spinal cord injury. All protocols were conducted with the approval of the Animal Ethics Committee of Zhengzhou University on March 16, 2019.
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http://dx.doi.org/10.4103/1673-5374.314323DOI Listing
January 2022

Platinum-Copper Bimetallic Colloid Nanoparticle Cluster Nanozymes with Multiple Enzyme-like Activities for Scavenging Reactive Oxygen Species.

Langmuir 2021 Jun 7. Epub 2021 Jun 7.

School of Chemistry and Chemical Engineering, Yangzhou University, Yangzhou, 225002 Jiangsu, P. R. China.

Fabrication of high-performance artificial antioxidant enzyme (AAE) systems based on a single nanozyme possessing multi-enzymatic activities is fascinating but challenging. Here, polyvinylpyrrolidone (PVP)-platinum-copper nanoparticle clusters (PVP-PtCuNCs) are prepared by a facile one-pot chemical coreduction method. PVP-PtCuNCs possess efficient superoxide dismutase (SOD)-like, peroxidase (POD)-like, and catalase (CAT)-like activities, and the multi-enzymatic activities depend on the bimetal component and cluster structure. Compared with individual platinum nanoparticle clusters (PVP-PtNCs), PVP-PtCuNCs can effectively eliminate reactive oxygen species (ROS) including superoxide anions, hydrogen peroxide, and hydroxyl radicals. The doping of copper not only reduces the usage of Pt content but also improves the catalytic efficiency and versatility effectively through the synergistic effect of bimetal components and the nanocluster structure. The results not only demonstrate that a single bimetallic nanozyme has the potential as an efficient AAE system in the biomedical application but also demonstrate that traditional concepts of structure-activity relationships can be used to fabricate nanozymes with the desired multi-enzymatic activities.
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http://dx.doi.org/10.1021/acs.langmuir.1c00697DOI Listing
June 2021

Damage to the blood‑brain barrier and activation of neuroinflammation by focal cerebral ischemia under hyperglycemic condition.

Int J Mol Med 2021 Jul 3;48(1). Epub 2021 Jun 3.

Department of Pathology, School of Basic Medical Science, Ningxia Medical University, Ningxia Key Laboratory of Cerebrocranial Diseases, Incubation Base of National Key Laboratory, Yinchuan, Ningxia 750004, P.R. China.

Hyperglycemia aggravates brain damage caused by cerebral ischemia/reperfusion (I/R) and increases the permeability of the blood‑brain barrier (BBB). However, there are relatively few studies on morphological changes of the BBB. The present study aimed to investigate the effect of hyperglycemia on BBB morphological changes following cerebral I/R injury. Streptozotocin‑induced hyperglycemic and citrate‑buffered saline‑injected normoglycemic rats were subjected to 30 min middle cerebral artery occlusion. Neurological deficits were evaluated. Brain infarct volume was assessed by 2,3,5‑triphenyltetrazolium chloride staining and BBB integrity was evaluated by Evans blue and IgG extravasation following 24 h reperfusion. Changes in tight junctions (TJ) and basement membrane (BM) proteins (claudin, occludin and zonula occludens‑1) were examined using immunohistochemistry and western blotting. Astrocytes, microglial cells and neutrophils were labeled with specific antibodies for immunohistochemistry after 1, 3 and 7 days of reperfusion. Hyperglycemia increased extravasations of Evan's blue and IgG and aggravated damage to TJ and BM proteins following I/R injury. Furthermore, hyperglycemia suppressed astrocyte activation and damaged astrocytic endfeet surrounding cerebral blood vessels following I/R. Hyperglycemia inhibited microglia activation and proliferation and increased neutrophil infiltration in the brain. It was concluded that hyperglycemia‑induced BBB leakage following I/R might be caused by damage to TJ and BM proteins and astrocytic endfeet. Furthermore, suppression of microglial cells and increased neutrophil infiltration to the brain may contribute to the detrimental effects of pre‑ischemic hyperglycemia on the outcome of cerebral ischemic stroke.
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http://dx.doi.org/10.3892/ijmm.2021.4975DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8175066PMC
July 2021

Low Surface Roughness Graphene Oxide Film Reduced with Aluminum Film Deposited by Magnetron Sputtering.

Nanomaterials (Basel) 2021 May 28;11(6). Epub 2021 May 28.

Tianjin Key Laboratory of Advanced Fibers and Energy Storage, School of Material Science and Engineering, Tiangong University, Tianjin 300387, China.

Graphene film has wide applications in optoelectronic and photovoltaic devices. A novel and facile method was reported for the reduction of graphene oxide (GO) film by electron transfer and nascent hydrogen produced between aluminum (Al) film deposited by magnetron sputtering and hydrochloric acid (HCl) solution for only 5 min, significantly shorter than by other chemical reduction methods. The thickness of Al film was controlled utilizing a metal detection sensor. The effect of the thickness of Al film and the concentration of HCl solution during the reduction was explored. The optimal thickness of Al film was obtained by UV-Vis spectroscopy and electrical conductivity measurement of reduced GO film. Atomic force microscope images could show the continuous film clearly, which resulted from the overlap of GO flakes, the film had a relatively flat surface morphology, and the surface roughness reduced from 7.68 to 3.13 nm after the Al reduction. The film sheet resistance can be obviously reduced, and it reached 9.38 kΩ/sq with a high transmittance of 80% (at 550 nm). The mechanism of the GO film reduction by electron transfer and nascent hydrogen during the procedure was also proposed and analyzed.
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http://dx.doi.org/10.3390/nano11061428DOI Listing
May 2021

Effect of hyperglycemia on microglial polarization after cerebral ischemia-reperfusion injury in rats.

Life Sci 2021 May 27;279:119660. Epub 2021 May 27.

Department of Pathology, School of Basic Medical Science, Ningxia Medical University, Ningxia Key Laboratory of Cerebrocranial Diseases, Incubation Base of National Key Laboratory, Yinchuan, Ningxia 750004, China. Electronic address:

Hyperglycemia has been shown to aggravate ischemic brain damage, in which the inflammatory reaction induced by hyperglycemia is involved in the worsening of cerebral ischemia-reperfusion injury. However, the role of microglial polarization in hyperglycemia-aggravating cerebral ischemia-reperfusion injury remains unknown. The present study investigated whether diabetic hyperglycemia inhibited or activated microglia, as well as microglial subtypes 1 and 2. Rats were used to establish the diabetic hyperglycemia and middle cerebral artery occlusion (MCAO) model. The markers CD11b, CD16, CD32, CD86, CD206, and Arg1 were used to show M1 or M2 microglia. The results revealed increased neurological deficits, infarct volume, and neural apoptosis in rats with hyperglycemia subjected to MCAO for 30 min and reperfused at 1, 3, and 7 days compared with the normoglycemic rats. Microglia and astrocyte activation and proliferation were inhibited in hyperglycemic rats. Furthermore, M1 microglia polarization was promoted, while that of M2 microglia was inhibited in hyperglycemic rats. These findings suggested that the polarization of M1 and M2 microglia is activated and inhibited, respectively, in hyperglycemic rats and may be involved in the aggravated brain damage caused by ischemia-reperfusion in diabetic hyperglycemia.
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http://dx.doi.org/10.1016/j.lfs.2021.119660DOI Listing
May 2021