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An innovative treatment for hypoxic-ischemic encephalopathy:Silk fibroin nanomaterials improve neural stem cell axon formation and facilitate cognitive improvement 认领 引用 被引量：1
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作者 Chao Han Shuna Chen +3 位作者 Zihan Shi Xin Guan Wei Zou Jing Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第7期3017-3025,共9页
Stem cell therapy shows promise for treating brain injuries;neural stem cells in particular are capable of repairing damage by forming new nerve cells and supporting recovery.However,optimizing the implantation and fu... Stem cell therapy shows promise for treating brain injuries;neural stem cells in particular are capable of repairing damage by forming new nerve cells and supporting recovery.However,optimizing the implantation and functionality of these cells in damaged brain regions remains challenging.Silk fibroin,a natural protein derived from silkworm silk,is a biocompatible material with exceptional properties that are useful for tissue engineering.Its biodegradability,mechanical robustness,and ability to promote cell growth make it particularly valuable for biomedical applications.Silk fibroin nanomaterials,which comprise silk fibroin processed into nanostructures,offer enhanced surface area,improved loading capacity for bioactive molecules,and superior nanoscale interactions with cells compared with bulk silk fibroin materials.In this study,we first extracted human-derived neural stem cells from a 14-week-old human fetus.Then,neural stem cells were loaded with 1%silk fibroin nanomaterials,which was identified as the optimal concentration to support human-derived neural stem cell growth and release of neurotrophic factors.Finally,1%silk fibroin nanomaterials were implanted into a rat model of hypoxic-ischemic brain injury.The results showed that,compared with the treatment with human-derived neural stem cells alone,silk fibroin hydrogel carrying human-derived neural stem cells was significantly more effective at alleviating brain tissue damage,increasing neurotrophic factor secretion in the brain microenvironment,and promoting motor and cognitive function recovery.These findings suggest that silk fibroin nanomaterials loaded with human-derived neural stem cells could be used to treat hypoxic-ischemic encephalopathy.However,the mechanisms and related signaling pathways by which hydrogels combined with cells exert their reparative effects still require further in-depth investigation. 展开更多
关键词 astrocyte deactivation axonal development cognitive recovery hypoxic-ischemic brain injury motor function nerve regeneration neural stem cells neurotrophic factor silk fibroin hydrogel synapse formation
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A blood-brain barrier-penetrative fluorescent probe revealing brain hypoxia damage in hypoxic-ischemic encephalopathy 认领 引用
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作者 Yuxun Lu Ning Zhu +9 位作者 Gui Zhang Huan Liu Le Yu Qisi Sun Ruqiu Zhang Xiaojuan Su Yinuo Li Zhenhui Li Fan Li Ying Zhou 《Chinese Chemical Letters》 SCIE CAS CSCD 2026年第6期507-513,共7页
Hypoxic-ischemic encephalopathy(HIE) is a major cause of infant mortality and permanent neurological abnormalities,highlighting the importance of early identification and accurate diagnosis.Fluorescence sensing provid... Hypoxic-ischemic encephalopathy(HIE) is a major cause of infant mortality and permanent neurological abnormalities,highlighting the importance of early identification and accurate diagnosis.Fluorescence sensing provides various benefits over traditional diagnostic methods,including real-time detection of hypoxia,which is often linked to HIE,and molecular-level insights.Herein,a novel hypoxia-responsive fluorescent probe,BOD,was created to overcome the difficulties associated with blood-brain barrier(BBB)penetration for brain damage imaging using a HIE model.BOD can be cleaved by azoreductase to produce a red fluorescent signal,with excellent sensitivity,selectivity,and biocompatibility.Crucially,BOD effectively monitors neural cells across varying oxygen concentrations,particularly in hypoxic microenvironments,providing vital insights into the impact of oxygen deprivation on neural cell function during HIE.In both cellular and ex vivo mouse brain tissue models,the effectiveness of BOD was confirmed:it outperformed conventional techniques in the reliable identification of hypoxic injury sites,differentiating between mild,moderate,and severe injury.Thanks to its excellent permeability due to its lipophilicity and positive charge,BOD can pass through the BBB,with strong fluorescence in the periventricular white matter(PWM) and cortex strongly correlated with injury severity.This study is novel in its application of a hypoxia-responsive fluorescent probe for brain damage imaging in an HIE model,highlighting the substantial potential of BOD for real-time,in vivo imaging,representing a promising tool for early diagnosis and investigation of HIE. 展开更多
关键词 Blood-brain barrier penetration Hypoxia-responsive Small-molecule fluorescent probe Neural cell imaging Hypoxic-ischemic encephalopathy
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Single-Nucleus RNA Sequencing Reveals the Mechanism of Neonatal Hypoxic-Ischemic Encephalopathy and the Neuroprotection Effects of Salvianolic Acid C 认领 引用
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作者 Xuan Mou Lu Li +9 位作者 Xinyue Liu Aolin Zhang Tao He Baofeng Rao Jiatian Zhang Renjie Chen Malte Spielmann Chi Chiu Wang Bin Cong Xiaohui Fan 《Engineering》 SCIE EI CSCD 2025年第12期269-290,共22页
Neonatal hypoxic-ischemic encephalopathy(HIE),resulting from perinatal asphyxia-induced hypoxic-ischemic brain damage(HIBD),is a severe neurological disorder that impairs neurodevelopment,and no definitive therapies a... Neonatal hypoxic-ischemic encephalopathy(HIE),resulting from perinatal asphyxia-induced hypoxic-ischemic brain damage(HIBD),is a severe neurological disorder that impairs neurodevelopment,and no definitive therapies are available.The polyphenolic natural compound salvianolic acid C(SAC)exhibits antioxidant,anti-inflammatory,and antiapoptotic properties.In this study,we evaluated the efficacy of SAC in treating HIE via animal and human brain organoid experiments.Human brain organoids served as a translational platform for assessing natural product efficacy and clinical effect prediction.Rat brain tissues were harvested at two time points(24 h and 7 d after HIBD and SAC administration)for single-nucleus RNA sequencing.In vitro and in vivo experiments,including microarrays and gene silencing,were employed to confirm the sequencing findings.Our findings demonstrated that during the acute phase of HIBD,SAC suppressed signal transducer and activator of transcription 3+(Stat3+)astrocyte-driven acute neuroinflammation,decreased inflammatory factor release,and maintained glial-immune homeostasis.During the subacute phase,SAC promoted oligodendrocyte differentiation and facilitated crosstalk between anti-inflammatory microglia and myelinating oligodendrocytes,establishing a regenerative microenvironment and enhancing neuregulin 3(NRG3)-receptor tyrosine-protein kinase erbB-4(ErbB4)signaling axis activity.These coordinated mechanisms highlight the dual capacity of SAC in mitigating early injury and driving structural repair in the later stages.This study revealed the pathophysiology of HIE and the multitarget neuroprotective effects of SAC against this disorder at single-cell resolution,advancing the mechanistic foundations for SAC-based therapies in neonatal brain injury. 展开更多
关键词 Neonatal hypoxic-ischemic encephalopathy Salvianolic acid C Human brain organoids Single-nucleus RNA sequencing
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Temporal dynamics of neonatal hypoxic-ischemic encephalopathy injuries on magnetic resonance imaging 认领 引用 被引量：1
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作者 Holly Flyger Samantha J.Holdsworth +2 位作者 Alistair J.Gunn Laura Bennet Hamid Abbasi 《Neural Regeneration Research》 SCIE CAS CSCD 2025年第11期3144-3150,共7页
Moderate to severe perinatal hypoxic-ischemic encephalopathy occurs in~1 to 3/1000 live births in high-income countries and is associated with a significant risk of death or neurodevelopmental disability.Detailed asse... Moderate to severe perinatal hypoxic-ischemic encephalopathy occurs in~1 to 3/1000 live births in high-income countries and is associated with a significant risk of death or neurodevelopmental disability.Detailed assessment is important to help identify highrisk infants,to help families,and to support appropriate interventions.A wide range of monitoring tools is available to assess changes over time,including urine and blood biomarkers,neurological examination,and electroencephalography.At present,magnetic resonance imaging is unique as although it is expensive and not suited to monitoring the early evolution of hypoxic-ischemic encephalopathy by a week of life it can provide direct insight into the anatomical changes in the brain after hypoxic-ischemic encephalopathy and so offers strong prognostic information on the long-term outcome after hypoxic-ischemic encephalopathy.This review investigated the temporal dynamics of neonatal hypoxic-ischemic encephalopathy injuries,with a particular emphasis on exploring the correlation between the prognostic implications of magnetic resonance imaging scans in the first week of life and their relationship to long-term outcome prediction,particularly for infants treated with therapeutic hypothermia.A comprehensive literature search,from 2016 to 2024,identified 20 pertinent articles.This review highlights that while the optimal timing of magnetic resonance imaging scans is not clear,overall,it suggests that magnetic resonance imaging within the first week of life provides strong prognostic accuracy.Many challenges limit the timing consistency,particularly the need for intensive care and clinical monitoring.Conversely,although most reports examined the prognostic value of scans taken between 4 and 10 days after birth,there is evidence from small numbers of cases that,at times,brain injury may continue to evolve for weeks after birth.This suggests that in the future it will be important to explore a wider range of times after hypoxic-ischemic encephalopathy to fully understand the optimal timing for predicting long-term outcomes. 展开更多
关键词 magnetic resonance imaging neonatal hypoxic-ischemic encephalopathy neurodevelopmental outcomes prognostic biomarkers in neuroimaging scan timing therapeutic hypothermia
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Resatorvid protects against hypoxic-ischemic brain damage in neonatal rats 认领 引用 被引量：24
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作者 Li-Jun Jiang Zhen-Xing Xu +5 位作者 Ming-Fu Wu Gai-Qin Dong Li-Li Zhang Jun-Yan Gao Chen-Xi Feng Xing Feng 《Neural Regeneration Research》 SCIE CAS CSCD 2020年第7期1316-1325,共10页
Secondary brain damage caused by hyperactivation of autophagy and inflammatory responses in neurons plays an important role in hypoxic-ischemic brain damage(HIBD).Although previous studies have implicated Toll-like re... Secondary brain damage caused by hyperactivation of autophagy and inflammatory responses in neurons plays an important role in hypoxic-ischemic brain damage(HIBD).Although previous studies have implicated Toll-like receptor 4(TLR4)and nuclear factor kappa-B(NF-κB)in the neuroinflammatory response elicited by brain injury,the role and mechanisms of the TLR4-mediated autophagy signaling pathway in neonatal HIBD are still unclear.We hypothesized that this pathway can regulate brain damage by modulating neuron autophagy and neuroinflammation in neonatal rats with HIBD.Hence,we established a neonatal HIBD rat model using the Rice-Vannucci method,and injected 0.75,1.5,or 3 mg/kg of the TLR4 inhibitor resatorvid(TAK-242)30 minutes after hypoxic ischemia.Our results indicate that administering TAK-242 to neonatal rats after HIBD could significantly reduce the infarct volume and the extent of cerebral edema,alleviate neuronal damage and neurobehavioral impairment,and decrease the expression levels of TLR4,phospho-NF-κB p65,Beclin-1,microtubule-associated protein l light chain 3,tumor necrosis factor-α,and interleukin-1βin the hippocampus.Thus,TAK-242 appears to exert a neuroprotective effect after HIBD by inhibiting activation of autophagy and the release of inflammatory cytokines via inhibition of the TLR4/NF-κB signaling pathway.This study was approved by the Laboratory Animal Ethics Committee of Affiliated Hospital of Yangzhou University,China(approval No.20180114-15)on January 14,2018. 展开更多
关键词 autophagy hypoxic-ischemic brain damage neonatal hypoxic-ischemic brain damage neuroinflammation nuclear factor kappa-B resatorvid TAK-242 Toll-like receptor 4
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Hyperbaric oxygen treatment promotes neural stem cell proliferation in the subventricular zone of neonatal rats with hypoxic-ischemic brain damage 认领 引用 被引量：18
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作者 Zhichun Feng Jing Liu Rong Ju 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第13期1220-1227,共8页
Hyperbaric oxygen therapy for the treatment of neonatal hypoxic-ischemic brain damage has been used clinically for many years, but its effectiveness remains controversial. In addition, the mechanism of this potential ... Hyperbaric oxygen therapy for the treatment of neonatal hypoxic-ischemic brain damage has been used clinically for many years, but its effectiveness remains controversial. In addition, the mechanism of this potential neuroprotective effect remains unclear. This study aimed to investigate the influence of hyperbaric oxygen on the proliferation of neural stem cells in the subventricular zone of neonatal Sprague-Dawley rats （7 days old） subjected to hypoxic-ischemic brain damage. Six hours after modeling, rats were treated with hyperbaric oxygen once daily for 7 days. Immunohistochemistry revealed that the number of 5-bromo-2＇-deoxyuridine positive and nestin positive cells in the subventricular zone of neonatal rats increased at day 3 after hypoxic-ischemic brain damage and peaked at day 5. After hyperbaric oxygen treatment, the number of 5-bromo-2＇- deoxyuddine positive and nestin positive cells began to increase at day 1, and was significantly higher than that in normal rats and model rats until day 21. Hematoxylin-eosin staining showed that hyperbaric oxygen treatment could attenuate pathological changes to brain tissue in neonatal rats, and reduce the number of degenerating and necrotic nerve cells. Our experimental findings indicate that hyperbaric oxygen treatment enhances the proliferation of neural stem cells in the subventricular zone of neonatal rats with hypoxic-ischemic brain damage, and has therapeutic potential for promoting neurological recovery following brain injury. 展开更多
关键词 neural regeneration brain injury neonatal hypoxic-ischemic encephalopathy hypoxic-ischemicbrain damage hyperbaric oxygen neural stem cells neurons proliferation subventricular zone neonatal rats nestin grants-supported paper neuroregeneration
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Research Progress on Exploring Biomarkers for Early Diagnosis of Neonatal Hypoxic-Ischemic Encephalopathy Based on Proteomics Technology 认领 引用
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作者 Zhaojun Geng Yumei Liang 《Journal of Clinical and Nursing Research》 2025年第7期435-440,共6页
Neonatal hypoxic-ischemic encephalopathy(HIE)refers to neonatal brain damage caused by various factors during the perinatal period that lead to hypoxia and reduced cerebral blood flow[1].Globally,0.2%to 2.26%of newbor... Neonatal hypoxic-ischemic encephalopathy(HIE)refers to neonatal brain damage caused by various factors during the perinatal period that lead to hypoxia and reduced cerebral blood flow[1].Globally,0.2%to 2.26%of newborns develop HIE,with approximately 20%resulting in neonatal death and about 25%of survivors suffering from neurological impairment[2].Currently,there is a lack of highly sensitive and specific diagnostic tools for HIE,posing significant challenges to reducing HIE mortality and neurological abnormalities[3].The development of high-throughput proteomics technology based on mass spectrometry(MS)has significantly enhanced the potential to discover biomarkers in biological fluids such as plasma,cerebrospinal fluid,saliva,and urine[4].Proteomics technology has become an engine for exploring novel markers of HIE[5].This article systematically reviews the progress of proteomics technology in the study of biomarkers for the early diagnosis of HIE,elucidating its potential application value. 展开更多
关键词 Neonatal hypoxic-ischemic encephalopathy Proteomics Biomarkers
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Neuroprotective effects of ginsenoside Rg1-induced neural stem cell transplantation on hypoxic-ischemic encephalopathy 认领 引用 被引量：21
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作者 Ying-bo Li Yan Wang +2 位作者 Ji-ping Tang Di Chen Sha-li Wang 《Neural Regeneration Research》 SCIE CAS CSCD 2015年第5期753-759,共7页
Ginsenoside Rgl is the major pharmacologically active component of ginseng, and is reported to have various therapeutic actions. To determine whether it induces the differentiation of neural stem cells, and whether ne... Ginsenoside Rgl is the major pharmacologically active component of ginseng, and is reported to have various therapeutic actions. To determine whether it induces the differentiation of neural stem cells, and whether neural stem cell transplantation after induction has therapeutic effects on hypoxic-ischemic encephalopathy, we cultured neural stem cells in 10-80 ~tM ginsenoside Rgl. Immunohistochemistry revealed that of the concentrations tested, 20 mM ginsenoside Rgl had the greatest differentiation-inducing effect and was the concentration used for subsequent exper- iments. Whole-cell patch clamp showed that neural stem cells induced by 20 jaM ginsenoside Rgl were more mature than non-induced cells. We then established neonatal rat models of hypox- ic-ischemic encephalopathy using the suture method, and ginsenoside Rgl-induced neural stem cells were transplanted via intracerebroventricular injection. These tests confirmed that neural stem cells induced by ginsenoside had fewer pathological lesions and had a significantly better behavioral capacity than model rats that received saline. Transplanted neural stem cells expressed neuron-specific enolase, and were mainly distributed in the hippocampus and cerebral cortex. The present data suggest that ginsenoside Rgl-induced neural stem cells can promote the partial recovery of complicated brain functions in models of hypoxic-ischemic encephalopathy. 展开更多
关键词 nerve regeneration hypoxic-ischemic brain damage ginsenoside Rgl neural stem cells cell transplantation ceil differentiation cognition nerve reconstruction neural regeneration
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Chlorogenic acid alleviates hypoxic-ischemic brain injury in neonatal mice 认领 引用 被引量：13
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作者 Lu-Yao Li Qi Wang +9 位作者 Lu Deng Zhen Lin Jing-Jing Lin Xin-Ye Wang Tian-Yang Shen Yi-Hui Zheng Wei Lin Pei-Jun Li Xiao-Qin Fu Zhen-Lang Lin 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第3期568-576,共9页
Recent studies have shown that chlorogenic acid(CGA),which is present in coffee,has protective effects on the nervous system.However,its role in neonatal hypoxic-ischemic brain injury remains unclear.In this study,we ... Recent studies have shown that chlorogenic acid(CGA),which is present in coffee,has protective effects on the nervous system.However,its role in neonatal hypoxic-ischemic brain injury remains unclear.In this study,we established a newborn mouse model of hypoxic-ischemic brain injury using a modified Rice-Vannucci method and performed intraperitoneal injection of CGA.We found that CGA intervention effectively reduced the volume of cerebral infarct,alleviated cerebral edema,restored brain tissue structure after injury,and promoted axon growth in injured brain tissue.Moreover,CGA pretreatment alleviated oxygen-glucose deprivation damage of primary neurons and promoted neuron survival.In addition,changes in ferroptosis-related proteins caused by hypoxic-ischemic brain injury were partially reversed by CGA.Furthermore,CGA intervention upregulated the expression of the key ferroptosis factor glutathione peroxidase 4 and its upstream glutamate/cystine antiporter related factors SLC7A11 and SLC3A2.In summary,our findings reveal that CGA alleviates hypoxic-ischemic brain injury in neonatal mice by reducing ferroptosis,providing new ideas for the treatment of neonatal hypoxic-ischemic brain injury. 展开更多
关键词 chlorogenic acid ferroptosis glutathione peroxidase 4 lipid peroxidation neonatal hypoxic-ischemic brain injury neurons neuroprotection oxidative stress oxygen-glucose deprivation system Xc-
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Mild hypothermia combined with neural stem cell transplantation for hypoxic-ischemic encephalopathy: neuroprotective effects of combined therapy 认领 引用 被引量：12
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作者 Lin Wang Feng Jiang +2 位作者 Qifeng Li Xiaoguang He Jie Ma 《Neural Regeneration Research》 SCIE CAS CSCD 2014年第19期1745-1752,共8页
Neural stem cell transplantation is a useful treatment for ischemic stroke, but apoptosis often occurs in the hypoxic-ischemic environment of the brain after cell transplantation. In this study, we determined if mild ... Neural stem cell transplantation is a useful treatment for ischemic stroke, but apoptosis often occurs in the hypoxic-ischemic environment of the brain after cell transplantation. In this study, we determined if mild hypothermia （27-28~C） can increase the survival rate of neural stem cells （1.0 x 105/~tL） transplanted into neonatal mice with hypoxic-ischemic encephalopathy. Long-term effects on neurological functioning of the mice were also examined. After mild hy- pothermia combined with neural stem cell transplantation, we observed decreased expression levels of inflammatory factor nuclear factor-kappa B and apoptotic factor caspase-3, reduced cerebral infarct volumes, increased survival rate of transplanted cells, and marked improvements in neurological function. Thus, the neuroprotective effects of mild hypothermia combined with neural stem cell transplantation are superior to those of monotherapy. Moreover, our findings suggest that the neuroprotective effects of mild hypothermia combined with neural stem cell transplantation on hypoxic-ischemic encephalopathy are achieved by anti-inflammatory and an- ti-apoptotic mechanisms. 展开更多
关键词 nerve regeneration brain injury hypoxic-ischemic encephalopathy neural precursorcells hypothermia neural stem cells cell transplantation hippocampus neuron cell apoptosis astrocytes oligodendrotytes neuroprotection NSFC grants neural regeneration
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Feasibility of allogeneic mesenchymal stem cells in pediatric hypoxic-ischemic encephalopathy: Phase I study 认领 引用 被引量：11
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作者 Serdar Kabatas Erdinç Civelek +7 位作者 Eyüp Can Savrunlu Necati Kaplan Osman Boyalı Furkan Diren Halil Can Ali Genç Tunç Akkoç Erdal Karaöz 《World Journal of Stem Cells》 SCIE 2021年第5期470-484,共15页
BACKGROUND Hypoxic-ischemic encephalopathy(HIE)is one of the leading causes of death and long-term neurological impairment in the pediatric population.Despite a limited number of treatments to cure HIE,stem cell thera... BACKGROUND Hypoxic-ischemic encephalopathy(HIE)is one of the leading causes of death and long-term neurological impairment in the pediatric population.Despite a limited number of treatments to cure HIE,stem cell therapies appear to be a potential treatment option for brain injury resulting from HIE.AIM To investigate the efficacy and safety of stem cell-based therapies in pediatric patients with HIE.METHODS The study inclusion criteria were determined as the presence of substantial deficit and disability caused by HIE.Wharton’s jelly-derived mesenchymal stem cells(WJ-MSCs)were intrathecally(IT),intramuscularly(IM),and intravenously administered to participants at a dose of 1×106/kg for each administration route twice monthly for 2 mo.In different follow-up durations,the effect of WJ-MSCs administration on HIE,the quality of life,prognosis of patients,and side effects were investigated,and patients were evaluated for neurological,cognitive functions,and spasticity using the Wee Functional Independence Measure(Wee FIM)Scale and Modified Ashworth(MA)Scale.RESULTS For all participants(n=6),the mean duration of exposure to hypoxia was 39.17+18.82 min,the mean time interval after HIE was 21.83±26.60 mo,the mean baseline Wee FIM scale score was 13.5±0.55,and the mean baseline MA scale score was 35±9.08.Three patients developed only early complications such as low-grade fever,mild headache associated with IT injection,and muscle pain associated with IM injection,all of which were transient and disappeared within 24 h.The treatment was evaluated to be safe and effective as demonstrated by magnetic resonance imaging examinations,electroencephalographies,laboratory tests,and neurological and functional scores of patients.Patients exhibited significant improvements in all neurological functions through a 12-mo follow-up.The mean Wee FIM scale score of participants increased from 13.5±0.55 to 15.17±1.6 points(mean±SD)at 1 mo(z=-1.826,P=0.068)and to 23.5±3.39 points at 12 mo(z=-2.207,P=0.027)post-treatment.The percentage of patients who achieved an excellent functional improvement(Wee FIM scale total score=126)increased from 10.71%(at baseline)to 12.03%at 1 mo and to 18.65%at 12 mo posttreatment.CONCLUSION Both the triple-route and multiple WJ-MSC implantations were safe and effective in pediatric patients with HIE with significant neurological and functional improvements.The results of this study support conducting further randomized,placebo-controlled studies on this treatment in the pediatric population. 展开更多
关键词 Hypoxic-ischemic encephalopathy Pediatric Stem cell Wharton jelly
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Transplantation of human placental chorionic plate-derived mesenchymal stem cells for repair of neurological damage in neonatal hypoxic-ischemic encephalopathy 认领 引用 被引量：5
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作者 Lulu Xue Ruolan Du +8 位作者 Ning Bi Qiuxia Xiao Yifei Sun Ruize Niu Yaxin Tan Li Chen Jia Liu Tinghua Wang Liulin Xiong 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第9期2027-2035,共9页
Neonatal hypoxic-ischemic encephalopathy is often associated with permanent cerebral palsy,neurosensory impairments,and cognitive deficits,and there is no effective treatment for complications related to hypoxic-ische... Neonatal hypoxic-ischemic encephalopathy is often associated with permanent cerebral palsy,neurosensory impairments,and cognitive deficits,and there is no effective treatment for complications related to hypoxic-ischemic encephalopathy.The therapeutic potential of human placental chorionic plate-derived mesenchymal stem cells for various diseases has been explored.However,the potential use of human placental chorionic plate-derived mesenchymal stem cells for the treatment of neonatal hypoxic-ischemic encephalopathy has not yet been investigated.In this study,we injected human placental chorionic plate-derived mesenchymal stem cells into the lateral ventricle of a neonatal hypoxic-ischemic encephalopathy rat model and observed significant improvements in both cognitive and motor function.Protein chip analysis showed that interleukin-3 expression was significantly elevated in neonatal hypoxic-ischemic encephalopathy model rats.Following transplantation of human placental chorionic plate-derived mesenchymal stem cells,interleukin-3 expression was downregulated.To further investigate the role of interleukin-3 in neonatal hypoxic-ischemic encephalopathy,we established an in vitro SH-SY5Y cell model of hypoxic-ischemic injury through oxygen-glucose deprivation and silenced interleukin-3 expression using small interfering RNA.We found that the activity and proliferation of SH-SY5Y cells subjected to oxygen-glucose deprivation were further suppressed by interleukin-3 knockdown.Furthermore,interleukin-3 knockout exacerbated neuronal damage and cognitive and motor function impairment in rat models of hypoxic-ischemic encephalopathy.The findings suggest that transplantation of hpcMSCs ameliorated behavioral impairments in a rat model of hypoxic-ischemic encephalopathy,and this effect was mediated by interleukin-3-dependent neurological function. 展开更多
关键词 behavioral evaluations gene knockout human neuroblastoma cells(SH-SY5Y) human placental chorionic derived mesenchymal stem cells interleukin-3 neonatal hypoxic-ischemic encephalopathy nerve injury oxygen-glucose deprivation protein chip small interfering RNA
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Thioperamide treats neonatal hypoxic-ischemic encephalopathy by postsynaptic H1 receptors 认领 引用 被引量：3
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作者 Feiyong Jia Lin Du +3 位作者 Yunpeng Hao Shicheng Liu Ning Li Huiyi Jiang 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第19期1814-1822,共9页
Thioperamide, a selective histamine H3 receptor antagonist, can increase histamine content in the brain, improve brain edema, and exert a neuroprotective effect. This study aimed to examine the mechanism of action of ... Thioperamide, a selective histamine H3 receptor antagonist, can increase histamine content in the brain, improve brain edema, and exert a neuroprotective effect. This study aimed to examine the mechanism of action of thioperamide during brain edema in a rat model of neonatal hypoxic ischemic encephalopathy. Our results showed that thioperamide significantly decreased brain water content and malondialdehyde levels, while significantly increased histamine levels and superoxide dismutase activity in the hippocampus. This evidence demonstrates that thioperamide could pre vent oxidative damage and attenuate brain edema following neonatal hypoxicischemic encepha Iopathy. We further observed that changes in the above indexes occurred after combined treatment of thioperamide with the H1 receptor antagonist, pyrilamine, and the H2 receptor antagonist, ci metidine. Experimental findings indicated that pyrilamine reversed the effects of thioperamide; however, cimetidine had no significant influence on the effects of thioperamide. Our present findings suggest that thioperamide can increase brain histamine content and attenuate brain edema and oxidative damage by acting in combination with postsynaptic H1 receptors in a rat model of neo natal hypoxicischemic encephalopathy. 展开更多
关键词 neural regeneration thioperamide histamine histamine receptor antagonist cimetidine pyrilamineneonatal hypoxic-ischemic encephalopathy brain edema hippocampus malondialdehyde super-oxide dismutase grants-supported paper neuroregeneration
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Time-dependent effect of combination therapy with erythropoietin and granulocyte colony-stimulating factor in a mouse model of hypoxic-ischemic brain injury 认领 引用 被引量：4
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作者 Ji Hea Yu Jung Hwa Seo +2 位作者 Jong Eun Lee Ji Hoe Heo Sung-Rae Cho 《Neuroscience Bulletin》 SCIE CAS CSCD 2014年第1期107-117,共11页
Erythropoietin （EPO） and granulocyte colony- stimulating factor （G-CSF） are likely to play broad roles in the brain. We investigated the effects of combination therapy with EPO and G-CSF in hypoxic- ischemic brain... Erythropoietin （EPO） and granulocyte colony- stimulating factor （G-CSF） are likely to play broad roles in the brain. We investigated the effects of combination therapy with EPO and G-CSF in hypoxic- ischemic brain injury during the acute, subacute, and chronic phases. A total of 79 C57BL/6 mice with hypoxic-ischemic brain injury were randomly assigned acute （days 1-5）, subacute （days 11-15）and chronic （days 28-32） groups. All of them were treated with G-CSF （250 μg/kg） and EPO （5 000 U/kg） or saline daily for 5 consecutive days. Behavioral assessments and immunohistochemistry for angiogenesis, neuro- genesis, and astrogliosis were performed with an 8-week follow-up. Hypoxia-inducible factor-1 （HIF-1） was also measured by Western blot analysis. The results showed that the combination therapy with EPO and G-CSF in the acute phase significantly improved rotarod performance and forelimb-use symmetry compared to the other groups, while subacute EPO and G-CSF therapy exhibited a modest improvement compared with the chronic saline controls. The acute treatment significantly increased the density of CD31^＋（PECAM-1） and a-smooth muscle actin^＋ vessels in the frontal cortex and striatum, increased BrdU^＋/PSA- NCAM^＋ neurogenesis in the subventricular zone, and decreased astroglial density in the striatum. Furthermore, acute treatment significantly increased the HIF-1 expression in the cytosol and nucleus, whereas chronic treatment did not change the HIF-1 expression, consistent with the behavioral outcomes. These results indicate that the induction of HIF-1 expression by combination therapy with EPO and G-CSF synergistically enhances not only behavioral function but also neurogenesis and angiogenesis while decreasing the astroglial response in a time- dependent manner. 展开更多
关键词 erythropoietin granulocyte colony-stimulating factor hypoxia-inducible factor-1 hypoxic-ischemic brain injury
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Human insulin-like growth factor 1-transfected umbilical cord blood neural stem cell transplantation improves hypoxic-ischemic brain injury 认领 引用 被引量：3
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作者 Dengna Zhu Yanjie Jia +3 位作者 Jun Wang Boai Zhang Guohui Niu Yazhen Fan 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第19期1445-1451,共7页
Human insulin-like growth factor 1-transfected umbilical cord blood neural stem cells were transplanted into a hypoxic-ischemic neonatal rat model via the tail vein. BrdU-positive cells at day 7 post-transplantation, ... Human insulin-like growth factor 1-transfected umbilical cord blood neural stem cells were transplanted into a hypoxic-ischemic neonatal rat model via the tail vein. BrdU-positive cells at day 7 post-transplantation, as well as nestin- and neuron specific enolase-positive cells at day 14 were increased compared with those of the single neural stem cell transplantation group. In addition, the proportion of neuronal differentiation was enhanced. The genetically modified cell-transplanted rats exhibited enhanced performance in correctly crossing a Y-maze and climbing an angled slope compared with those of the single neural stem cell transplantation group. These results showed that human insulin-like growth factor 1-transfected neural stem cell transplantation promotes the recovery of the leaming, memory and motor functions in hypoxic-ischemic rats. 展开更多
关键词 human insulin-like growth factor 1 neural stem cell hypoxic-ischemic brain damage transplantation neural regeneration
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Preclinical anti-apoptotic properties of salidroside for hypoxic-ischemic cerebral damage:a systematic review and meta-analysis 认领 引用 被引量：2
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作者 WANG Xiaobo ZHANG Yating +4 位作者 HOU Ya JIANG Hong ZHANG Yi ZHANG Sanyin MENG Xianli 《Digital Chinese Medicine》 CAS CSCD 2023年第2期121-135,共15页
Objective As the main active ingredient of Tibetan medicine Hongjingtian(Rhodiolae Crenulatae Radix et Rhizoma),salidroside(Sal)has a good anti-apoptotic potential.Currently,there are some conflicting results on the a... Objective As the main active ingredient of Tibetan medicine Hongjingtian(Rhodiolae Crenulatae Radix et Rhizoma),salidroside(Sal)has a good anti-apoptotic potential.Currently,there are some conflicting results on the anti-apoptotic mechanisms of Sal.Here we conducted a systematic review and meta-analysis to provide the preclinical evidence of its anti-apoptotic properties in preventing and treating hypoxic-ischemic cerebral damage(HICD).Methods The literature on the anti-apoptotic potential of Sal in the treatment of HICD from January 1,1980 to November 9,2021 was searched online using Chinese databases including Chinese National Knowledge Infrastructure(CNKI),China Science and Technology Journal Database(VIP),and Wanfang Database,and English databases including PubMed and Web of Science.The quality of the included articles was evaluated by the Cochrane Collaboration network bias risk assessment criteria,and meta-analysis was performed using RevMan 5.3 software.Results A total of 40 articles were finally included.Among the 40 articles,30 were about in vivo animal experiments and 17 about in vitro cell experiments,and 7 of them included both animal and cell experiments.After analysis,it was found that Sal had significant effects on disease-related indicators of HICD(P<0.05),such as cerebral infarctsize and brain water content.As to in vivo studies,Sal mainly affects the expressions of apoptotic factors through antiinflammation,anti-oxidation,activation of complement pathway,and regulation of signal transduction and autophagy,thus exerting anti-apoptotic potential in treating HICD.While for in vitro studies,Sal plays the anti-apoptotic role in HICD models mainly through anti-oxidation,anti-inflammation,reduction of Ca2+overload,regulation of mitochondrial function,signal transduction,and C3 complement.Conclusion Sal can take anti-apoptotic effects to prevent and treat HICD through mechanisms such as anti-inflammation,anti-oxidation,enhanced autophagy,complement and signal transduction,regulation of mitochondrial membrane potential,and reduction of Ca2+overload. 展开更多
关键词 Salidroside Hypoxic-ischemic cerebral damage Apoptosis Preclinical Anti-oxidation Ca2+overload
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Phase I study on the safety and preliminary efficacy of allogeneic mesenchymal stem cells in hypoxic-ischemic encephalopathy 认领 引用 被引量：5
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作者 Serdar Kabataş ErdinçCivelek +9 位作者 Necati Kaplan Eyüp Can Savrunlu Gülseli Berivan Sezen Mourat Chasan Halil Can Ali Genç Yener Akyuva Osman Boyalı Furkan Diren Erdal Karaoz 《World Journal of Experimental Medicine》 2021年第2期17-29,共13页
BACKGROUND Hypoxic-ischemic encephalopathy(HIE)is a leading cause of morbidity and mortality in the adult as well as in the neonate,with limited options for treatment and significant dysfunctionality.AIM To investigat... BACKGROUND Hypoxic-ischemic encephalopathy(HIE)is a leading cause of morbidity and mortality in the adult as well as in the neonate,with limited options for treatment and significant dysfunctionality.AIM To investigate the safety and preliminary efficacy of allogeneic mesenchymal stem cells(MSCs)in HIE patients.METHODS Patients who had HIE for at least 6 mo along with significant dysfunction and disability were included.All patients were given Wharton’s jelly-derived MSCs at 1×106/kg intrathecally,intravenously,and intramuscularly twice a month for two months.The therapeutic effects and prognostic implications of MSCs were evaluated by multiple follow-ups.Functional independence measure(FIM),modified Ashworth,and Karnofsky scales were used to assess any side effects,neurological and cognitive functions,and overall outcomes.RESULTS The 8 subjects included in the study had a mean age of 33.25±10.18 years.Mean HIE exposure and mean post-HIE durations were 45.63±10.18 and 19.67±29.04 mo,respectively.Mean FIM score was 18.38±1.06,mean modified Ashworth score was 43.5±4.63,and mean Karnofsky score was 20.For the first 24 h,5 of the patients experienced a subfebrile state,accompanied by mild headaches due to intrathecally administration and muscle pain because of intramuscularly administration.Neurological and functional examinations,laboratory tests,electroencephalography,and magnetic resonance imaging were performed to assess safety of treatment.Mean FIM score increased by 20.88±3.31 in the first month(P=0.027)and by 31.38±14.69 in 12 mo(P=0.012).The rate of patients with an FIM score of 126 increased from 14.58%to 16.57%in the first month and 24.90%in 12 mo.CONCLUSION Multiple triple-route Wharton’s jelly-derived MSC administrations were found to be safe for HIE patients,indicating neurological and functional improvement.Based on the findings obtained here,further randomized and placebo research could be performed. 展开更多
关键词 Hypoxic-ischemic encephalopathy Stem cell Transplantation Wharton's jelly
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Meta-analysis evaluation of the treatment of neonatal hypoxic-ischemic encephalopathy with ganglioside 认领 引用 被引量：2
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作者 Wen LI Junli YANG +2 位作者 Dong ZHOU Jinghui ZHANG Qingcui ZHUO 《BIOCELL》 SCIE 2019年第1期7-11,共5页
The efficacy and safety of ganglioside in the treatment of neonates who suffer from hypoxic-ischemic encephalopathy(HIE)needs to be fully evaluated.We searched the following databases:PubMed,ScienceDirect,LISTA,CNKI,C... The efficacy and safety of ganglioside in the treatment of neonates who suffer from hypoxic-ischemic encephalopathy(HIE)needs to be fully evaluated.We searched the following databases:PubMed,ScienceDirect,LISTA,CNKI,Chinese biomedical literature database and Wanfang digital journals of full-text database to determine the inclusion and exclusion criteria of papers and a total of 12 papers were included after quality evaluation.Then we conducted the meta-analysis with RevMan5.0 software.The results showed that compared with the control group,the abnormal rate declined in the ganglioside-treated group(relative risk(RR)=0.27,95%confidence interval(CI)=0.05-1.96).NBNA records of the 7,10-14d neonates were improved effectively:RR(95%CI)were 2.28(0.86-3.42)and 2.53(1.04-2.92)respectively.Neural system sequelae incidence was reduced significantly:RR(95%CI)=0.35:(0.15-0.79).Ganglioside treatment could effectively reduce the abnormality rate of head size,improve the neurological score,reduce the incidence of neurological sequelae,and significantly prompt clinical recovery for neonates with HIE. 展开更多
关键词 Ganglioside Hypoxic-ischemic encephalopathy Meta-analysis Neonate
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AD-16 Protects Against Hypoxic-Ischemic Brain Injury by Inhibiting Neuroinflammation 认领 引用 被引量：1
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作者 Zhihua Huang Zhengwei Luo +5 位作者 Andrea Ovcjak Jiangfan Wan Nai-hong Chen Wenhui Hu Hong-Shuo Sun Zhong-Ping Feng 《Neuroscience Bulletin》 SCIE CAS CSCD 2022年第8期857-870,共14页
Neuroinflammation is a key contributor to the pathogenic cascades induced by hypoxic-ischemic(HI)insult in the neonatal brain.AD-16 is a novel anti-inflammatory compound,recently found to exert potent inhibition of th... Neuroinflammation is a key contributor to the pathogenic cascades induced by hypoxic-ischemic(HI)insult in the neonatal brain.AD-16 is a novel anti-inflammatory compound,recently found to exert potent inhibition of the lipopolysaccharide-induced production of pro-inflammatory and neurotoxic mediators.In this study,we evaluated the effect of AD-16 on primary astrocytes and neurons under oxygen-glucose deprivation(OGD)in vitro and in mice with neonatal HI brain injury in vivo.We demonstrated that AD-16 protected against OGD-induced astrocytic and neuronal cell injury.Single dose post-treatment with AD-16(1 mg/kg)improved the neurobehavioral outcome and reduced the infarct volume with a therapeutic window of up to 6 h.Chronic administration reduced the mortality rate and preserved whole-brain morphology following neonatal HI.The in vitro and in vivo effects suggest that AD-16 offers promising therapeutic efficacy in attenuating the progression of HI brain injury and protecting against the associated mortality and morbidity. 展开更多
关键词 Neuroinflammation Neonatal hypoxic-ischemic brain injury Neuroprotection AD-16
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Estrogen inhibits lipid peroxidation after hypoxic-ischemic brain damage in neonatal rats 认领 引用 被引量：2
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作者 Hui Zhu Xiao Han +2 位作者 Dafeng Ji Guangming Lv Meiyu Xu 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第31期2424-2431,共8页
Sprague-Dawley neonatal rats within 7 days after birth were used in this study. The left common carotid artery was occluded and rats were housed in an 8% O2 environment for 2 hours to establish a hypoxic-ischemic brai... Sprague-Dawley neonatal rats within 7 days after birth were used in this study. The left common carotid artery was occluded and rats were housed in an 8% O2 environment for 2 hours to establish a hypoxic-ischemic brain damage model. 17β-estradiol （1 × 10-5 M） was injected into the rat abdominal cavity after the model was successfully established. The left hemisphere was obtained at 12, 24, 48, 72 hours after operation. Results showed that malondialdehyde content in the left brain of neonatal rats gradually increased as modeling time prolonged, while malondialdehyde content of 17β-estrodial-treated rats significantly declined by 24 hours, reached lowest levels at 48 hours, and then peaked at 72 hours after injury. Nicotinamide-adenine dinucleotide phosphate histochemical staining showed the nitric oxide synthase-positive cells and fibers dyed blue/violet and were mainly distributed in the cortex, hippocampus and medial septal nuclei. The number of nitric oxide synthase-positive cells peaked at 48 hours and significantly decreased after 17β-estrodial treatment. Our experimental findings indicate that estrogen plays a protective role following hypoxic-ischemic brain damage by alleviating lipid peroxidation through reducing the expression of nitric oxide synthase and the content of malondialdehyde. 展开更多
关键词 hypoxic-ischemic encephalopathy hypoxic-ischemic brain damage estrogen malondialdehyde free radical nitric oxide synthase lipid peroxidation neonatal rats neuroprotection neural regeneration
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