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Synapsing with NG2 cells(polydendrocytes),unappreciated barrier to axon regeneration? 被引量:2
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作者 Young-Jin Son 《Neural Regeneration Research》 SCIE CAS CSCD 2015年第3期346-348,共3页
Have you heard of NG2 cells or NG2 glia or polydendro- cytes~. These are new names for the precursor cells that used to be referred to as oligodendrocyte precursor cells (OPCs), which become the oligodendrocytes tha... Have you heard of NG2 cells or NG2 glia or polydendro- cytes~. These are new names for the precursor cells that used to be referred to as oligodendrocyte precursor cells (OPCs), which become the oligodendrocytes that myelinate central nervous system (CNS) axons. Evidence suggests, however, that they have other functions, besides differentiating into oligodendrocytes. Most notably, the OPCs/NG2 cells are uni- formly distributed in grey matter as well as in white matter, which matches poorly with the distribution of myelinating oligodendrocytes. Furthermore, not every NG2 cell is fated to become an oligodendrocyte. Hence the term OPC can be fairly applied only when discussing the role of these cells in the oligodendrocyte lineage. 展开更多
关键词 NG CELL Synapsing with NG2 cells polydendrocytes unappreciated barrier to axon regeneration
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Microscale tissue-engineered models:overcoming barriers to adoption for neural regeneration research 被引量:1
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作者 Michael J.Moore 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第3期386-387,共2页
The last decade has seen a steady proliferation in the use of tissue-engineered cell culture systems(Deforest and Anseth,2012),and these have been put to good use for studying neural axon growth and guidance(Li and... The last decade has seen a steady proliferation in the use of tissue-engineered cell culture systems(Deforest and Anseth,2012),and these have been put to good use for studying neural axon growth and guidance(Li and Hoffman-Kim,2008;Roy et al.,2013).These systems have been designed to more closely mimic the natural microenvironment of the developing or repairing nervous system and to enable spatiotemporal control over certain aspects of the microenvironment. 展开更多
关键词 engineered regeneration adoption barriers mimic enable guidance projection friendly overcome
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Propofol protects against blood-spinal cord barrier disruption induced by ischemia/reperfusion injury 被引量:14
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作者 Li-jie Xie Jin-xiu Huang +4 位作者 Jian Yang Fen Yuan Shuang-shuang Zhang Qi-jing Yu Ji Hu 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第1期125-132,共8页
Propofol has been shown to exert neuroprotective effects on the injured spinal cord.However,the effect of propofol on the blood-spinal cord barrier(BSCB) after ischemia/reperfusion injury(IRI) is poorly understood... Propofol has been shown to exert neuroprotective effects on the injured spinal cord.However,the effect of propofol on the blood-spinal cord barrier(BSCB) after ischemia/reperfusion injury(IRI) is poorly understood.Therefore,we investigated whether propofol could maintain the integrity of the BSCB.Spinal cord IRI(SCIRI) was induced in rabbits by infrarenal aortic occlusion for 30 minutes.Propofol,30 mg/kg,was intravenously infused 10 minutes before aortic clamping as well as at the onset of reperfusion.Then,48 hours later,we performed histological and m RNA/protein analyses of the spinal cord.Propofol decreased histological damage to the spinal cord,attenuated the reduction in BSCB permeability,downregulated the m RNA and protein expression levels of matrix metalloprotease-9(MMP-9) and nuclear factor-κB(NF-κB),and upregulated the protein expression levels of occludin and claudin-5.Our findings suggest that propofol helps maintain BSCB integrity after SCIRI by reducing MMP-9 expression,by inhibiting the NF-κB signaling pathway,and by maintaining expression of tight junction proteins. 展开更多
关键词 nerve regeneration spinal cord ischemia reperfusion injury blood–spinal cord barrier propofol matrix metalloprotease-9 nuclear factor-κB tight junction proteins neural regeneration
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Non-viral liposome-mediated transfer of brain-derived neurotrophic factor across the blood-brain barrier 被引量:8
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作者 Ying Xing Chun-yan Wen +1 位作者 Song-tao Li Zong-xin Xia 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第4期617-622,共6页
Brain-derived neurotrophic factor(BDNF) plays an important role in the repair of central nervous system injury,but cannot directly traverse the blood-brain barrier.Liposomes are a new type of non-viral vector,able t... Brain-derived neurotrophic factor(BDNF) plays an important role in the repair of central nervous system injury,but cannot directly traverse the blood-brain barrier.Liposomes are a new type of non-viral vector,able to carry macromolecules across the blood-brain barrier and into the brain.Here,we investigate whether BDNF could be transported across the blood-brain barrier by tail-vein injection of liposomes conjugated to transferrin(Tf) and polyethylene glycol(PEG),and carrying BDNF modified with cytomegalovirus promoter(pC MV) or glial fibrillary acidic protein promoter(p GFAP)(Tf-p CMV-BDNF-PEG and Tf-p GFAP-BDNF-PEG,respectively).Both liposomes were able to traverse the blood-brain barrier,and BDNF was mainly expressed in the cerebral cortex.BDNF expression in the cerebral cortex was higher in the Tf-p GFAP-BDNF-PEG group than in the Tf-p CMV-BDNF-PEG group.This study demonstrates the successful construction of a non-virus targeted liposome,Tf-p GFAP-BDNF-PEG,which crosses the blood-brain barrier and is distributed in the cerebral cortex.Our work provides an experimental basis for BDNF-related targeted drug delivery in the brain. 展开更多
关键词 nerve regeneration brain injury brain-derived neurotrophic factor liposomes targeting vector transfection hippocampus cortex encapsulation efficiency blood-brain barrier transferrin glial fibrillary acidic protein polyethylene glycol neural regeneration
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Exploiting kinase polypharmacology for nerve regeneration
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作者 Hassan Al-Ali John L.Bixby Vance P.Lemmon 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第1期71-72,共2页
The human central nervous system(CNS)has a markedly poor capacity for regenerating its axons following injury.This appears to be due to two main causes:1)a developmentally regulated decline in regenerative capacit... The human central nervous system(CNS)has a markedly poor capacity for regenerating its axons following injury.This appears to be due to two main causes:1)a developmentally regulated decline in regenerative capacity within mature CNS neurons,and 2)the presence of biological components that constitute barriers to axon regeneration(e.g.,growth-inhibitory molecules). 展开更多
关键词 regeneration alterations mature markedly constitute regenerative barriers phenotypic similarity inhibit
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Dexamethasone prevents vascular damage in earlystage non-freezing cold injury of the sciatic nerve 被引量:1
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作者 Hao Li Lei Zhang Min Xu 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第1期163-167,共5页
Non-freezing cold injury is a prevalent cause of peripheral nerve damage, but its pathogenic mechanism is poorly understood, and treatment remains inadequate. Glucocorticoids have anti-inflammatory and lipid peroxidat... Non-freezing cold injury is a prevalent cause of peripheral nerve damage, but its pathogenic mechanism is poorly understood, and treatment remains inadequate. Glucocorticoids have anti-inflammatory and lipid peroxidation-inhibiting properties. We therefore examined whether dexamethasone, a synthetic glucocorticoid compound, would alleviate early-stage non-freezing cold injury of the sciatic nerve. We established Wistar rat models of non-freezing cold injury by exposing the left sciatic nerve to cold(3–5°C) for 2 hours, then administered dexamethasone(3 mg/kg intraperitoneally) to half of the models. One day after injury, the concentration of Evans blue tracer in the injured sciatic nerve of rats that received dexamethasone was notably lower than that in the injured sciatic nerve of rats that did not receive dexamethasone; neither Evans blue dye nor capillary stenosis was observed in the endoneurium, but myelinated nerve fibers were markedly degenerated in the injured sciatic nerve of animals that received dexamethasone. After dexamethasone administration, however, endoneurial vasculopathy was markedly improved, although damage to the myelinated nerve fiber was not alleviated. These findings suggest that dexamethasone protects the blood-nerve barrier, but its benefit in non-freezing cold injury is limited to the vascular system. 展开更多
关键词 nerve regeneration peripheral nerve injury sciatic nerve hypothermia blood-nerve barrier non-freezing cold injury dexamethasone neural regeneration
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3′-Daidzein sulfonate sodium improves mitochondrial functions after cerebral ischemia/reperfusion injury 被引量:10
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作者 Wa Yuan Qin Chen +4 位作者 Jing Zeng Hai Xiao Zhi-hua Huang Xiao Li Qiong Lei 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第2期235-241,共7页
3′-Daidzein sulfonate sodium is a new synthetic water-soluble compound derived from daidzein(an active ingredient of the kudzu vine root). It has been shown to have a protective effect on cerebral ischemia/reperfus... 3′-Daidzein sulfonate sodium is a new synthetic water-soluble compound derived from daidzein(an active ingredient of the kudzu vine root). It has been shown to have a protective effect on cerebral ischemia/reperfusion injury in rats. We plan to study the mechanism of its protective effect. 3′-Daidzein sulfonate sodium was injected in rats after cerebral ischemia/reperfusion injury. Results showed that 3′-daidzein sulfonate sodium significantly reduced mitochondrial swelling, significantly elevated the mitochondrial membrane potential, increased mitochondrial superoxide dismutase and glutathione peroxidase activities, and decreased mitochondrial malondialdehyde levels. 3′-Daidzein sulfonate sodium improved the structural integrity of the blood-brain barrier and reduced blood-brain barrier permeability. These findings confirmed that 3′-daidzein sulfonate sodium has a protective effect on mitochondrial functions after cerebral ischemia/reperfusion injury, improves brain energy metabolism, and provides protection against blood-brain barrier damage. 展开更多
关键词 nerve regeneration 3′-daidzein sulfonate sodium cerebral ischemia/reperfusion injury infarct volume anti-oxidation mitochondria mitochondrial membrane swelling mitochondrial membrane potential superoxide dismutase malondialdehyde glutathione peroxidase blood-brain barrier neural regeneration
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