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Scutellarin protects oxygen/glucose-deprived astrocytes and reduces focal cerebral ischemic injury 被引量:17
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作者 Jing-Bo Sun Yan Li +11 位作者 Ye-Feng Cai Yan Huang Shu Liu Patrick KK Yeung Min-Zhen Deng Guang-Shun Sun Prince LM Zilundu Qian-Sheng Hu Rui-Xin An Li-Hua Zhou Li-Xin Wang Xiao Cheng 《Neural Regeneration Research》 SCIE CAS CSCD 2018年第8期1396-1407,共12页
Scutellarin, a bioactive flavone isolated from Scutellaria baicalensis, has anti-inflammatory, anti-neurotoxic, anti-apoptotic and anti-oxida- tive effects and has been used to treat cardiovascular and cerebrovascular... Scutellarin, a bioactive flavone isolated from Scutellaria baicalensis, has anti-inflammatory, anti-neurotoxic, anti-apoptotic and anti-oxida- tive effects and has been used to treat cardiovascular and cerebrovascular diseases in China. However, the mechanisms by which scutellarin mediates neuroprotection in cerebral ischemia remain unclear. The interaction between scutellarin and nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) was assessed by molecular docking study, which showed that scutellarin selectively binds to NOX2 with high affinity. Cultures of primary astrocytes isolated from the cerebral cortex of neonatal Sprague-Dawley rats were pretreated with 2, 10 or 50 μM scutellarin for 30 minutes. The astrocytes were then subjected to oxygen/glucose deprivation by incubation for 2 hours in glucose-free Dulbecco's modified Eagle's medium in a 95% N2/5% CO2 incubator, followed by simulated reperfusion for 22 hours. Cell viability was assessed by cell counting kit-8 assay. Expression levels of NOX2, connexin 43 and caspase-3 were assessed by western blot assay. Reactive oxygen species were measured spectrophotometrically. Pretreatment with 10 or 50 μM scutellarin substantially increased viability, reduced the expression of NOX2 and caspase-3, increased the expression of connexin 43, and diminished the levels of reactive oxygen, species in astrocytes subjected to ischemia-'reperfusion. We also assessed the effects of scutellarin in vivo in the rat transient middle cerebral artery occlusion model of cerebral ischemia-reperfusion injury. Rats were given intraperitoneal injection of 100 mg/kg scutellarin 2 hours before surgery. The Bederson scale was used to assess neurological deficit, and 2,3,5-triphenyltetrazolium chloride staining was used to measure infarct size. Western blot assay was used to assess expression of NOX2 and connexin 43 in brain tissue. Enzyme-linked immunosorbent assay was used to detect 8-hydroxydeoxyguanosine (8-OHdG), 4-hydroxy-2-nonenal (4-HNE) and 3-nitrotyrosin (3-NT) in brain tissue. Immunofluorescence double staining was used to determine the co-expression of caspase-3 and NeuN. Pretreatment with scutellarin im- proved the neurological function of rats with focal cerebral ischemia, reduced infarct size, diminished the expression of NOX2, reduced levels of 8-OHdG, 4-HNE and 3-NT, and reduced the number of cells co-expressing caspase-3 and NeuN in the injured brain tissue. Furthermore, we examined the effect of the NOX2 inhibitor apocynin. Apocynin substantially increased connexin 43 expression in vivo and in vitro. Collectively, our findings suggest that scutellarin protects against ischemic injury in vitro and in vivo by downregulating NOX2, upregulating connexin 43, decreasing oxidative damage, and reducing apoptotic cell death. 展开更多
关键词 nerve regeneration SCUTELLARIN cerebral ischemic injury oxygen glucose deprivation/reoxygenation nicotinamide adenine dinucleotide phosphate oxidase 2 reactive oxygen species connexin 43 neural regeneration
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Acupuncture activates signal transduction pathways related to brain-tissue restoration after ischemic injury 被引量:9
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作者 Haomei Tian Hong Zhang +4 位作者 Junbao Zhu Juan Zhang Hening Cai Yuchen Zhang Chutao Chen 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第24期1866-1872,共7页
A middle cerebral artery occlusion-model was established in rats using the improved thread embolism method.Rats were treated with acupuncture at either Dazhui(DU14),Renzhong(DU26), Baihui(DU20),or a non-meridian... A middle cerebral artery occlusion-model was established in rats using the improved thread embolism method.Rats were treated with acupuncture at either Dazhui(DU14),Renzhong(DU26), Baihui(DU20),or a non-meridian point.Detection with protein-chip technology showed that the level of protein phosphorylation in both groups was upregulated or downregulated depending on the signaling pathway compared with the model group that did not receive acupuncture.Analysis of proteins showing downregulated phosphorylation revealed that five signaling pathways were activated in the acupuncture-treatment group,while only two were activated in the acupuncture-control group.In contrast,analysis of proteins showing upregulated phosphorylation revealed only one pathway was activated in the acupuncture-treatment group,whereas four pathways were activated in the acupuncture-control group.Furthermore,the number of activated proteins in the acupuncture-treatment group was not only higher than the acupuncture-control group,but unlike the acupuncture-control group,the majority of activated proteins were key proteins in the signaling pathways.Our findings indicate that acupuncture at specific points can activate multiple signaling pathways to promote the restoration of brain tissue following ischemic injury,and that this is based on a combination of effects resulting from multiple pathways,targets,and means. 展开更多
关键词 ACUPUNCTURE cerebral ischemia DAZHUI Baihui RENZHONG protein-chip technology signal-transduction pathways nerve injury brain injury ischemic injury neural regeneration
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Blood microRNAs as potential diagnostic and prognostic markers in cerebral ischemic injury 被引量:11
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作者 Bridget Martinez Philip V.Peplow 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第9期1375-1378,共4页
MicroRNAs are a family of small, genome-encoded endogenous RNAs that are transcribed but are not translated into proteins. They serve essential roles in virtually every aspect of brain function, including neurogenesis... MicroRNAs are a family of small, genome-encoded endogenous RNAs that are transcribed but are not translated into proteins. They serve essential roles in virtually every aspect of brain function, including neurogenesis, neural development, and cellular responses leading to changes in synaptic plasticity. They are also implicated in neurodegeneration and neurological disorders, in responses to hypoxia and ischemia, and in ischemic tolerance induced by ischemic preconditioning. In recent developments, miRNA expres- sion profiling has been examined in stroke, and these studies indicate that miRNAs have emerged as key mediators in ischemic stroke biology. Both increased and decreased miRNA levels may be needed either as prevention or treatment of stroke. Novel approaches are being developed to get miRNA related therapeu- tics into the brain across an intact blood-brain barrier, including chemical modification, use of targeting molecules and methods to disrupt the blood-brain barrier. 展开更多
关键词 blood microRNAs diagnostic biomarkers prognostic biomarkers cerebral ischemic injury ischemicstroke human patients rat and mouse models
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Prevention and protection against cerebral ischemic injury using acupuncture 被引量:3
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作者 Philip V.Peplow Bridget Martinez 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第4期559-560,共2页
Cardiovascular disease is the leading cause of death worldwide.Stroke is the second leading cause of death above the age of 60 years and the leading cause of acquired disability in adults.The main type of stroke is is... Cardiovascular disease is the leading cause of death worldwide.Stroke is the second leading cause of death above the age of 60 years and the leading cause of acquired disability in adults.The main type of stroke is ischemic stroke(80%)and it is subclassified as thrombotic or embolic in nature. 展开更多
关键词 TIA MCAO Prevention and protection against cerebral ischemic injury using acupuncture TBI TLT PBP EA
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Controlling N-methyl-D-aspartate receptor subunit 1 with calcitonin gene related peptide after cerebral ischemic injury
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作者 Jixiang Cui1, Peng Qu2, Chunping Qiao3 1Department of Clinical Laboratory, Fourth Affiliated Hospital of China Medical University, Shenyang 110032, Liaoning Province, China 2Department of Neurobiology, Basic Medical College of China Medical University, Shenyang 110032, Liaoning Province, China 3Department of Emergency, Baicheng Central Hospital of Jilin Province, Baicheng 137000, Jilin Province, China 《Neural Regeneration Research》 SCIE CAS CSCD 2006年第7期585-588,共4页
BACKGROUND: Activation of N-methyl-D-aspartate receptor (NMDAR) is a key link of exitotoxicity at the phase of cerebral ischemic injury. Because NMDAR is a main way to mediate internal flow of Ca2+ among glutamic acid... BACKGROUND: Activation of N-methyl-D-aspartate receptor (NMDAR) is a key link of exitotoxicity at the phase of cerebral ischemic injury. Because NMDAR is a main way to mediate internal flow of Ca2+ among glutamic acid receptors, over-excitation can cause neuronal apoptosis. Calcitonin gene related peptide has a strongly biological activity. On one hand, it can protect ischemic neurons through inhibiting the expression of NMDAR1 mRNA; on the other hand, it can play the protective effect through down-regulating the expression of NMDAR1 mRNA by exogenous calcitonin gene related peptide. OBJECTIVE: To observe the expression of NMDAR1 and the regulatory effect of calcitonin gene related peptide on the expression of NMDAR1 mRNA and protein in the cerebral cortex of rats with focal cerebral ischemia/reperfusion (I/R). DESIGN: Randomized controlled animal study. SETTING: China Medical University. MATERIALS: A total of 216 healthy male Wistar rats, general grade, weighing 250-280 g, were selected in this study. Twelve rats were randomly selected to regard as control group; meanwhile, other 204 rats were used to establish middle cerebral artery occlusion/reperfusion (MACO) models. The main reagents were detailed as follows: calcitonin gene related peptide (Sigma Company); calcitonin gene related peptide kit (Boster Company); antibody Ⅰ, Ⅱ and antibody β-actin Ⅰ, Ⅱ of NMDAR1 mRNA and chemiluminescence reagent (Santa Cruz Company, USA). METHODS: The experiment was carried out in the Laboratory of Neurobiology of China Medical University from August 2005 to June 2006. ① Right MCAO models of rats were established to cause focal ischemia and scored based on Zea Longa five-grade scale. If the scores were 1, 2 and 3 after wakefulness, the MACO models were established successfully and involved in the experiment. A total of 120 rats with successful modeling were randomly divided into I/R group and administration group with 60 in each group. All rats in the both groups were observed at five time points, including 6, 12, 24, 48 and 72 hours after reperfusion and after 2-hour ischemia, with 12 experimental animals at each time point. Six rats were prepared for detection of hybridization in situ, and the other 6 were used for Western blotting histochemical detection. Rats in the control group were opened their skin to separate common carotid artery and not treated with line and drugs. In addition, rats in the I/R group were treated with 1 mL saline at 2 hours after focal cerebral ischemia, and then, rats in the administration group were treated with 1 mL (1 g/L) calcitonin gene related peptide at 2 hours after focal cerebral ischemia. ② The expression of NMDAR1 mRNA was detected with hybridization in situ at various time points; moreover, the expression of NMDAR1 protein was measured with Western blotting method at various time points. The results were analyzed with Metamoph imaging analytical system. MAIN OUTCOME MEASURES: The expression of NMDAR1 mRNA and its protein in cortical neurons of rats at various time points. RESULTS: A total of 84 rats were excluded because of non-symptoms, exanimation or death; and then, 132 rats were involved in the final analysis. The expression of NMDAR1 mRNA and its protein in cortical neurons of rats in the control group was 0.205±0.001 and 0.184±0.001, respectively; after I/R, expression of NMDAR1 mRNA and its protein was up-regulated, especially, expression of mRNA at 6, 12, 24, 48 and 72 hours was 0.245±0.003, 0.287±0.004, 0.354±0.008, 0.284±0.002 and 0.217±0.006, respectively; moreover, expression of protein at 6, 12, 24, 48 and 72 hours was 0.222±0.003, 0.261±0.028, 0.311±0.004, 0.259±0.013 and 0.210±0.008, respectively. There was significant difference between the two groups (0.205±0.001, P < 0.01). The expression was up-related in the former 24 hours, reached peak at 24 hours, down-regulated, and decreased to the level of control group at 72 hours. Except 72 hours, the expression of NMDAR1 mRNA and its protein was lower in administration group than that in I/R group at other four time points. In addition, the expression of mRNA at 6, 12, 24, 48 and 72 hours was 0.223±0.005, 0.243±0.001, 0.292±0.002, 0.250±0.003 and 0.213±0.003, respectively; moreover, the expression of protein at 6, 12, 24, 48 and 72 hours was 0.216±0.006, 0.245±0.025, 0.276±0.003, 0.241±0.045 and 0.202±0.013, respectively. There was significant difference at various time points (P < 0.05). CONCLUSION: The expressions of NMDAR1 mRNA and its protein of peripheral cortical neurons are up-related in ischemic area after focal cerebral I/R. Meanwhile, exogenous calcitonin gene related peptide can protect cortical neurons through inhibiting expression of NMDAR1 mRNA and its protein after focal cerebral I/R. 展开更多
关键词 NMDAR MRNA Controlling N-methyl-D-aspartate receptor subunit 1 with calcitonin gene related peptide after cerebral ischemic injury GENE
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Effects of NG-nitro-L-arginine on focal cerebral ischemic injury in rats
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作者 Jianxin Zhang Huixin Zhang Lanfang Li Yonghui Li 《Neural Regeneration Research》 SCIE CAS CSCD 2006年第1期40-43,共4页
BACKGROUND: Previous researches have proved that aminoguanidin can cure cerebral ischemic injury remarkably as a selective induced nitricoxide synthase (iNOS) inhibitor. However, whether nonselective NOS inhibitor ... BACKGROUND: Previous researches have proved that aminoguanidin can cure cerebral ischemic injury remarkably as a selective induced nitricoxide synthase (iNOS) inhibitor. However, whether nonselective NOS inhibitor could protect cerebral ischemic injury or not is unclear. OBJECTIVE: To investigate the effects of NG-nitro-L-arginine (L-NA), a nonselective nitricoxide synthase (NOS) inhibitor, on cerebral ischemic injury of rats and the possible mechanism.DESIGN: Randomized controlled study.SETTING : Pharmacological Department of Medical Academy of Science of Hebei Province.MATERIALS: A total of 56 male healthy SD rats, of grade Ⅱ, weighting 250-290 g, were provided by the Experimental Animal Center of Hebei Province (certification: 04036). METHODS: The experiment was completed in the Pharmacological Department of Medical Academy of Science of Hebei Province from March 2005 to January 2006.① Grouping: Rats were randomly divided into 3 groups: sham operation group (n=8), model group (n=24) and L-NA group (n=24).② Modeling: Middle cerebral artery (MCA) was established on rats in model group and L-NA group with intreluminal line occlusion methods, and rats in sham operation group were separated their external carotid arteries without occlusion of internal carotid artery. ③ Intervention study: Rats in model group and L-NA group were injected intreperitoneally with 10 mL/kg and 20 mg/kg L-NA at 2, 6 and 12 hours respectively after ischemia twice a day for 3 consecutive days. ④ Rats were sacrificed on the third day for measuring volume of cerebral infarction with image analysis and swelling degrees and activities of mitochondria with electron microscope. Effect of L-NA on ultrastructural changes of neurons in cortex was observed after ischemia. MAIN OUTCOME MEASURES:① Volume of cerebral infarction; ②Swelling degrees, contents of nitric oxide (NO) and malondialdehyde (MDA) and activities of adenosine triphosphatase (ATPase), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in mitochondria;③ Ultrastructural changes of mitochondria in brain tissue after cerebral ischemia. RESULTS: ① At 12 hour after ischemia, volume of cerebral infarction in L-NA group was lower than that in model group (P 〈 0.01). ② Content of NO in mitochondria in L-NA group was decreased as compared with that in model group at 2, 6 and 12 hours after ischemia (P 〈 0.05); swelling degree of mitochondria in brain tissue was relieved in L-NA group at 12 hour after ischemia, and content of MDA was decreased (P 〈 0.05); mitochondrial activity in L-NA group was increased at 12 hour after ischemia, and activities of ATPase, SOD and GSH-Px in mitochondria were increased (P 〈 0.05).③ Degrees of mitochondrial injury in brain tissue were relieved in L-NA group at 12 hour after ischemia as compared with those in model group and L-NA group at 2 and 6 hours after ischemia. CONCLUSION : ①L-NA can beneficially inhibit NO production, but not protect brain against damage in ischemia acute stage. ②L-NA might have protective effects on cerebral injury through inhibiting the production of oxygen free radical, increasing antioxidation, ameliorating energy metabolism, beneficially improving the integrity of form and function of mitochondria in brain tissue during postischemia in rats. 展开更多
关键词 Effects of NG-nitro-L-arginine on focal cerebral ischemic injury in rats NG
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Acupuncture promotes repair of cerebral ischemic injury
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《Neural Regeneration Research》 SCIE CAS CSCD 2012年第30期2354-2354,共1页
Three articles conceming the molecular biology and proteomics study of the mechanism underlying the effects of acupuncture on the repair of cerebral ischemic injury were published in the Neural Regeneration Research. ... Three articles conceming the molecular biology and proteomics study of the mechanism underlying the effects of acupuncture on the repair of cerebral ischemic injury were published in the Neural Regeneration Research. We hope that our readers find these papers useful to their research. 展开更多
关键词 Acupuncture promotes repair of cerebral ischemic injury
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S100B protein in serum is elevated after global cerebral ischemic injury 被引量:9
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作者 Bao-di Sun Hong-mei Liu Shi-nan Nie 《World Journal of Emergency Medicine》 CAS 2013年第3期165-168,共4页
BACKGROUND:S100B protein in patients with cardiac arrest,hemorrhagic shock and other causes of global cerebral ischemic injury will be dramatically increased.Ischemic brain injury may elevate the level of serum S100 B... BACKGROUND:S100B protein in patients with cardiac arrest,hemorrhagic shock and other causes of global cerebral ischemic injury will be dramatically increased.Ischemic brain injury may elevate the level of serum S100 B protein and the severity of brain damage.METHODS:This article is a critical and descriptive review on S100 B protein in serum after ischemic brain injury.We searched Pubmed database with key words or terms such as "S100B protein", "cardiac arrest", "hemorrhagic shock" and "ischemia reperfusion injury" appeared in the last five years.RESULTS:S100B protein in patients with cardiac arrest,hemorrhagic shock and other causes of ischemic brain injury will be dramatically increased.Ischemic brain injury elevated the level of serum S100 B protein,and the severity of brain damage.CONCLUSION:The level of S100 B protein in serum is elevated after ischemic brain injury,but its mechanism is unclear. 展开更多
关键词 S100B ischemic brain injury Cardiac arrest Hemorrhagic shock
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Neuroimmunomodulatory effects of transcranial laser therapy combined with intravenous tPA administration for acute cerebral ischemic injury 被引量:2
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作者 Philip V.Peplow 《Neural Regeneration Research》 SCIE CAS CSCD 2015年第8期1186-1190,共5页
At present, the only FDA approved treatment for ischemic strokes is intravenous administration of tissue plasminogen activator within 4.5 hours of stroke onset. Owing to this brief window only a small percentage of pa... At present, the only FDA approved treatment for ischemic strokes is intravenous administration of tissue plasminogen activator within 4.5 hours of stroke onset. Owing to this brief window only a small percentage of patients receive tissue plasminogen activator. Transcranial laser therapy has been shown to be effective in animal models of acute ischemic stroke, resulting in significant improvement in neurological score and function. NEST-1 and NEST-2 clinical trials in human patients have demonstrated the safety and positive trends in efficacy of transcranial laser therapy for the treatment of ischemic stroke when initiated close to the time of stroke onset. Combining intravenous tissue plasminogen activator treatment with transcranial laser therapy may provide better functional outcomes. Statins given within 4 weeks of stroke onset improve stroke outcomes at 90 days compared to patients not given statins, and giving statins following transcranial laser therapy may provide an effective treatment for patients not able to be given tissue plasminogen activator due to time constraints. 展开更多
关键词 ischemic stroke inflammation injury cellular changes laser therapy neuromodulation
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The miR-9-5p/CXCL11 pathway is a key target of hydrogen sulfide-mediated inhibition of neuroinflammation in hypoxic ischemic brain injury 被引量:2
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作者 Yijing Zhao Tong Li +6 位作者 Zige Jiang Chengcheng Gai Shuwen Yu Danqing Xin Tingting Li Dexiang Liu Zhen Wang 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第5期1084-1091,共8页
We previously showed that hydrogen sulfide(H2S)has a neuroprotective effect in the context of hypoxic ischemic brain injury in neonatal mice.However,the precise mechanism underlying the role of H2S in this situation r... We previously showed that hydrogen sulfide(H2S)has a neuroprotective effect in the context of hypoxic ischemic brain injury in neonatal mice.However,the precise mechanism underlying the role of H2S in this situation remains unclear.In this study,we used a neonatal mouse model of hypoxic ischemic brain injury and a lipopolysaccharide-stimulated BV2 cell model and found that treatment with L-cysteine,a H2S precursor,attenuated the cerebral infarction and cerebral atrophy induced by hypoxia and ischemia and increased the expression of miR-9-5p and cystathionineβsynthase(a major H2S synthetase in the brain)in the prefrontal cortex.We also found that an miR-9-5p inhibitor blocked the expression of cystathionineβsynthase in the prefrontal cortex in mice with brain injury caused by hypoxia and ischemia.Furthermore,miR-9-5p overexpression increased cystathionine-β-synthase and H2S expression in the injured prefrontal cortex of mice with hypoxic ischemic brain injury.L-cysteine decreased the expression of CXCL11,an miR-9-5p target gene,in the prefrontal cortex of the mouse model and in lipopolysaccharide-stimulated BV-2 cells and increased the levels of proinflammatory cytokines BNIP3,FSTL1,SOCS2 and SOCS5,while treatment with an miR-9-5p inhibitor reversed these changes.These findings suggest that H2S can reduce neuroinflammation in a neonatal mouse model of hypoxic ischemic brain injury through regulating the miR-9-5p/CXCL11 axis and restoringβ-synthase expression,thereby playing a role in reducing neuroinflammation in hypoxic ischemic brain injury. 展开更多
关键词 chemokine(C-X-C motif)ligand 11 cystathionineβsynthase H2S hypoxic ischemic brain injury inflammation L-CYSTEINE lipopolysaccharide microglia miR-9-5p neuroprotection
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Effect of Qingre Huayu Decoction on Autophagy and Apoptosis of Neurons in Rats with Ischemic Brain Injury by Regulating Ca^(2+)/CaMKKβ-AMPK-mTOR Pathway
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作者 Qun TONG Xuelan KUANG +2 位作者 Jinfeng ZHOU Jinhua YUAN Xianjing ZENG 《Medicinal Plant》 2024年第5期39-43,共5页
[Objectives]To explore the neuroprotective mechanism of Qingre Huayu Decoction on rats with acute cerebral ischemia injury.[Methods]SD rats were divided into sham operation group,ischemia model group,low,medium and hi... [Objectives]To explore the neuroprotective mechanism of Qingre Huayu Decoction on rats with acute cerebral ischemia injury.[Methods]SD rats were divided into sham operation group,ischemia model group,low,medium and high dose groups of Qingre Huayu De-coction,with 10 rats in each group.Referring to the MCAO operation model,both the sham operation group and the model group were given normal saline by gavage,and the Qingre Huayu Decoction group was given different doses of Qingre Huayu Decoction by gavage.After the op-eration,the rats were scored for neurological deficit,neurons were stained with HE,apoptotic cells were detected with TUNEL,and the levels of autophagy and apoptotic proteins in the Ca^(2+)/CaMKKβ-AMPK-mTORpathway in brain tissue were detected with Western-blot.[Results]Compared with the model group,the neurological function score of Qingre Huayu Decoction Group decreased significantly(P<0.05),the pathological damage of neurons in Qingre Huavu Decoction Group decreased.the proportion of apoptosis-positive cells detected by TUNEL de-creased(P<0.05),and the expression of CaMKKβand AMPK increased,expression of mTOR decreased,expression of Beclin-1 and LC3 increased,and expression of Caspase-3decreased in Qingre Huayu Decoction Group(P<0.05).[Conclusions]Qingre Huayu Decoction may play a neuroprotective role by activating Ca^(2+)/CaMKKβ-AMPK-mTOR pathway and regulating the level of apoptosis and autophagy. 展开更多
关键词 Qingre Huayu Decoction ischemic brain injury Apoptosis Autophagy
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Cell polarization in ischemic stroke: molecular mechanisms and advances
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作者 Yuanwei Li Xiaoxiao Xu +5 位作者 Xuan Wu Jiarui Li Shiling Chen Danyang Chen Gaigai Li Zhouping Tang 《Neural Regeneration Research》 SCIE CAS 2025年第3期632-645,共14页
Ischemic stroke is a cerebrovascular disease associated with high mortality and disability rates. Since the inflammation and immune response play a central role in driving ischemic damage, it becomes essential to modu... Ischemic stroke is a cerebrovascular disease associated with high mortality and disability rates. Since the inflammation and immune response play a central role in driving ischemic damage, it becomes essential to modulate excessive inflammatory reactions to promote cell survival and facilitate tissue repair around the injury site. Various cell types are involved in the inflammatory response, including microglia, astrocytes, and neutrophils, each exhibiting distinct phenotypic profiles upon stimulation. They display either proinflammatory or anti-inflammatory states, a phenomenon known as ‘cell polarization.’ There are two cell polarization therapy strategies. The first involves inducing cells into a neuroprotective phenotype in vitro, then reintroducing them autologously. The second approach utilizes small molecular substances to directly affect cells in vivo. In this review, we elucidate the polarization dynamics of the three reactive cell populations(microglia, astrocytes, and neutrophils) in the context of ischemic stroke, and provide a comprehensive summary of the molecular mechanisms involved in their phenotypic switching. By unraveling the complexity of cell polarization, we hope to offer insights for future research on neuroinflammation and novel therapeutic strategies for ischemic stroke. 展开更多
关键词 astrocyte polarization immune regulation inflammation ischemic injury microglia polarization neutrophil polarization signaling pathways STROKE
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Morphological and functional observations of a novel model of retinal ischemia injury induced by bilateral carotid artery stenosis in mice
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作者 Lian Shu You-Jia Zhang +1 位作者 Xiao-Xiao Chen Xing-Huai Sun 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2024年第12期2192-2202,共11页
AIM:To investigate the features of retinal ischemic injuries in a novel mouse model with bilateral carotid artery stenosis(BCAS).METHODS:BCAS was induced with microcoil implantation in 6-8-week-old C57BL6 mice.Cerebra... AIM:To investigate the features of retinal ischemic injuries in a novel mouse model with bilateral carotid artery stenosis(BCAS).METHODS:BCAS was induced with microcoil implantation in 6-8-week-old C57BL6 mice.Cerebral blood flow was monitored at 2,7,and 28d postoperatively.Retinal morphological changes were evaluated by fundus photography and hematoxylin-eosin staining.Fluorescein fundus angiography(FFA)was performed to detect retinal vascular changes and circulation.The levels of apoptosis,activation of neurogliosis,and expression of hypoxiainducible factor(HIF)-1αin the retina were assessed by Western blotting and immunofluorescence staining,followed by retinal ganglion cell(RGC)density detection.Additionally,electrophysiological examinations including photopic negative response(PhNR)was also performed.RESULTS:The mice demonstrated an initial rapid decrease in cerebral blood flow,followed by a 4-week recovery period after BCAS.The ratio of retinal artery and vein was decreased under fundus photography and FFA.Compared with the sham mice,BCAS mice showed thinner retinal thickness on day 28.Additionally,apoptosis was increased and RGC density was decreased mainly in peripheral retinal region.Neurogliosis was mainly located in the inner retinal layers,with a stable increase in HIF-1αexpression.The dark-adapted electroretinogram showed a notable reduction in the a-,b-,and oscillatory potential(OP)wave amplitudes between days 2 and 7;this gradually recovered over the following 4wk.However,the b-and OPwave amplitudes were still significantly decreased on PhNR examination on day 28.CONCLUSION:BCAS can result in relatively mild retinal ischemia injuries in mice,mainly in the inner layer and peripheral region.Our study provides a novel animal model for investigating retinal ischemic diseases. 展开更多
关键词 bilateral carotid artery stenosis retinal ischemia MICE cerebral hypoperfusion ischemic injury
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Curcumin protects against ischemic spinal cord injury The pathway effect 被引量:9
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作者 Jinhua Zhang Hao Wei +3 位作者 Meimei Lin Chunmei Chen Chunhua Wang Maobai Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第36期3391-3400,共10页
Inducible nitric oxide synthase and N-methyI-D-aspartate receptors have been shown to participate in nerve cell injury during spinal cord ischemia. This study observed a protective effect of curcumin on ischemic spina... Inducible nitric oxide synthase and N-methyI-D-aspartate receptors have been shown to participate in nerve cell injury during spinal cord ischemia. This study observed a protective effect of curcumin on ischemic spinal cord injury. Models of spinal cord ischemia were established by ligating the lumbar artery from the left renal artery to the bifurcation of the abdominal aorta. At 24 hours after model establishment, the rats were intraperitoneally injected with curcumin, Reverse transcrip- tion-polymerase chain reaction and immunohistochemical results demonstrated that after spinal cord ischemia, inducible nitric oxide synthase and N-methyI-D-aspartate receptor mRNA and protein expression significantly increased. However, curcumin significantly decreased inducible nitric oxide synthase and N-methyI-D-aspartate receptor mRNA and protein expression in the ischemic spinal cord. Tadov scale results showed that curcumin significantly improved motor function of the rat hind limb after spinal cord ischemia. The results demonstrate that curcumin exerts a neuroprotective ef- fect against ischemic spinal cord injury by decreasing inducible nitric oxide synthase and N-methyI-D-aspartate receptor expression. 展开更多
关键词 neural regeneration traditional Chinese medicine CURCUMIN spinal cord injury ischemic injury N-methyI-D-aspartate receptor inducible nitric oxide synthase NEUROPROTECTION grants-supported paper NEUROREGENERATION
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Hypothermia ameliorates gastrointestinal ischemic injury sustained in a porcine cardiac arrest model 被引量:4
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作者 LU Yi WANG Shuo LI Chun-sheng 《Chinese Medical Journal》 SCIE CAS CSCD 2012年第24期4406-4411,共6页
Background During cardiac arrest, the gastrointestinal tract is sensitive to ischemia. Protection of the gastrointestinal tract is a critical factor in determining prognosis following cardiopulmonary resuscitation (... Background During cardiac arrest, the gastrointestinal tract is sensitive to ischemia. Protection of the gastrointestinal tract is a critical factor in determining prognosis following cardiopulmonary resuscitation (CPR). This study seeks to determine the extent of gastrointestinal tract injury and the potential protective effect of inducing hypothermia following a porcine cardiac arrest model and CPR. Methods Ventricular fibrillation was induced by programmed electrical stimulation in 16 male domestic pigs (n=8 per group). Four minutes after ventricular fibrillation, CPR was performed. Pigs that successfully restored spontaneous circulation then received intravenous infusions of saline at either 4℃ or room temperature to produce hypothermic and control conditions respectively. Serum diamine oxidase and gastrointestinal adenosine triphosphate enzyme activity were determined and histopathology of the gastrointestinal tract was performed by light microscopy and electron microscopy. Results Significant injury of the gastrointestinal tract after CPR was found. Na+-K+ and Ca2+ adenosine triphosphate enzyme activity in the gastric tissue were significantly high in animals receiving hypothermia treatment compared to controls. Hypothermia also significantly reduced serum diamine oxidase after CPR compared to the control group. Moreover, severe injury sustained by the gastrointestinal tissue was significantly ameliorated under hypothermic conditions compared to controls. Conclusions Gastrointestinal injury and abnormal energy metabolism are strikingly evident following CPR. Hypothermia, which is induced by an infusion of 4℃ saline, can rapidly reduce internal body temperature, improve energy metabolism, and ameliorate injury to the gastrointestinal mucosa after CPR. 展开更多
关键词 cardiac arrest cardiopulmonary resuscitation gastrointestinal tract HYPOTHERMIA ischemic injury
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EFFECT OF WARM ISCHEMIC INJURY ON MORPHOLOGY AND VIABILITY OF AORTIC VALVES IN RATS
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作者 陈钢 刘维永 俞世强 《Chinese Medical Journal》 SCIE CAS CSCD 1995年第1期24-27,共4页
Warm ischemia is one of the most important causes of valvular damage from death of donor to its valve harvesting. This study aimed at using qualitative and quantitative methods to characterize warm ischemic injury thr... Warm ischemia is one of the most important causes of valvular damage from death of donor to its valve harvesting. This study aimed at using qualitative and quantitative methods to characterize warm ischemic injury through models of SD rat's aortic valves and design to show the relationship among ultrastructural, biological and biochemical changes concerning with the length of warm ischemia time (WIT). 102 harvested SD rat's aortic valves were divided into 6 groups of different ischemic time for this study. 432 photomicrographs of transmission electron microscopy (TEM) were put into computer for analysis. The volume ratio of nucleus to plasma in cells (Vnp) and the ratio of extramembrane area to volume of mitochondria (S / V) were used to characterize the degree of valvular cell injuries. Valvular cells culture and biochemical metabolism including glucose degredation and H-3-TdR absorption rate were adopted. The valvular cells depicted a significant decrease and H-3-TdR taking-up also being inhibited under the influence of prolonged WIT. 展开更多
关键词 WIT In EFFECT OF WARM ischemic injury ON MORPHOLOGY AND VIABILITY OF AORTIC VALVES IN RATS
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Therapeutic application of chick early amniotic fluid: effective rescue of acute myocardial ischemic injury by intravenous administration
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作者 Baiping Cui Yufan Zheng +14 位作者 Xiang Gao Lihong Zhang Borui Li Jia Chen Xinyan Zhou Mengyuan Cai Wenrui Sun Yuting Zhang Keejong Chang Jiayi Xu Fuyin Zhu Yan Luo Tao Sun Jin Qian Ning Sun 《Cell Regeneration》 2022年第1期84-96,共13页
Myocardial regeneration has been considered a promising option for the treatment of adult myocardial injuries.Previously,a chick early amniotic fluid(ceAF)preparation was shown to contain growth-related factors that p... Myocardial regeneration has been considered a promising option for the treatment of adult myocardial injuries.Previously,a chick early amniotic fluid(ceAF)preparation was shown to contain growth-related factors that pro-moted embryonic growth and cellular proliferation,though the nature of the components within ceAF were not fully defined.Here we tested whether this ceAF preparation is similarly effective in the promotion of myocardial regen-eration,which could provide an alternative therapeutic for intervening myocardial injury.In this study,a myocardial ischemic injury model was established in adult mice and pigs by multiple research entities,and we were able to show that ceAF can efficiently rescue damaged cardiac tissues and markedly improve cardiac function in both experimental models through intravenous administration.ceAF administration increased cell proliferation and improved angio-genesis,likely via down-regulation of Hippo-YAP signaling.Our data suggest that ceAF administration can effectively rescue ischemic heart injury,providing the key functional information for the further development of ceAF for use in attenuating myocardial injury. 展开更多
关键词 Myocardial ischemic injury Chick early amniotic fluid HEART Yap
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Dabrafenib,an inhibitor of RIP3 kinase-dependent necroptosis,reduces ischemic brain injury 被引量:17
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作者 Shelly A.Cruz Zhaohong Qin +1 位作者 Alexandre E R.Stewart Hsiao-Huei Chen 《Neural Regeneration Research》 SCIE CAS CSCD 2018年第2期252-256,共5页
Ischemic brain injury triggers neuronal cell death by apoptosis via caspase activation and by necroptosis through activation of the receptor-interacting protein kinases (RIPK) associated with the tumor necrosis fact... Ischemic brain injury triggers neuronal cell death by apoptosis via caspase activation and by necroptosis through activation of the receptor-interacting protein kinases (RIPK) associated with the tumor necrosis factor-alpha (TNF-a)/death receptor. Recent evidence shows RIPK inhibitors are neuroprotective and al- leviate ischemic brain injury in a number of animal models, however, most have not yet undergone clinical trials and safety in humans remains in question. Dabrafenib, originally identified as a B-raf inhibitor that is currently used to treat melanoma, was later revealed to be a potent RIPK3 inhibitor at micromolar con- centrations. Here, we investigated whether Dabrafenib would show a similar neuroprotective effect in mice subjected to ischemic brain injury by photothrombosis. Dabrafenib administered intraperitoneally at 10 mg/ kg one hour after photothrombosis-induced focal ischemic injury significantly reduced infarct lesion size in C57BL6 mice the following day, accompanied by a markedly attenuated upregulation of TNF-u. However, subsequent lower doses (5 mg/kg/day) failed to sustain this neuroprotective effect after 4 days. Dabrafenib bl ocked lipopolysaccharides-induced activation of TNF-ct in bone marrow-derived macrophages, suggesting that Dabrafenib may attenuate TNF-ct-induced necroptotic pathway after ischemic brain injury. Since Dab- rafenib is already in clinical use for the treatment of melanoma, it might be repurposed for stroke therapy. 展开更多
关键词 ischemic brain injury inflammation MACROPHAGE Dabrafenib tumor necrosis factor-alpha PHOTOTHROMBOSIS receptor-interacting protein kinases NECROPTOSIS microgIia stroke neural regeneration
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Modeling subcortical ischemic white matter injury in rodents:unmet need for a breakthrough in translational research 被引量:3
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作者 Yuexian Cui Xuelian Jin +1 位作者 Jun Young Choi Byung Gon Kim 《Neural Regeneration Research》 SCIE CAS CSCD 2021年第4期638-642,共5页
Subcortical ischemic white matter injury(SIWMI),pathological correlate of white matter hyperintensities or leukoaraiosis on magnetic resonance imaging,is a common cause of cognitive decline in elderly.Despite its high... Subcortical ischemic white matter injury(SIWMI),pathological correlate of white matter hyperintensities or leukoaraiosis on magnetic resonance imaging,is a common cause of cognitive decline in elderly.Despite its high prevalence,it remains unknown how various components of the white matter degenerate in response to chronic ischemia.This incomplete knowledge is in part due to a lack of adequate animal model.The current review introduces various SIWMI animal models and aims to scrutinize their advantages and disadvantages primarily in regard to the pathological manifestations of white matter components.The SIWMI animal models are categorized into 1)chemically induced SIWMI models,2)vascular occlusive SIWMI models,and 3)SIWMI models with comorbid vascular risk factors.Chemically induced models display consistent lesions in predetermined areas of the white matter,but the abrupt evolution of lesions does not appropriately reflect the progressive pathological processes in human white matter hyperintensities.Vascular occlusive SIWMI models often do not exhibit white matter lesions that are sufficiently unequivocal to be quantified.When combined with comorbid vascular risk factors(specifically hypertension),however,they can produce progressive and definitive white matter lesions including diffuse rarefaction,demyelination,loss of oligodendrocytes,and glial activation,which are by far the closest to those found in human white matter hyperintensities lesions.However,considerable surgical mortality and unpredictable natural deaths during a follow-up period would necessitate further refinements in these models.In the meantime,in vitro SIWMI models that recapitulate myelinated white matter track may be utilized to study molecular mechanisms of the ischemic white matter injury.Appropriate in vivo and in vitro SIWMI models will contribute in a complementary manner to making a breakthrough in developing effective treatment to prevent progression of white matter hyperintensities. 展开更多
关键词 animal model axonal degeneration DEMYELINATION hypertension ischemia OLIGODENDROCYTES subcortical ischemic white matter injury vascular cognitive impairment white matter hyperintensities
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Vascular endothelial growth factor: an attractive target in the treatment of hypoxic/ischemic brain injury 被引量:15
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作者 Hui Guo Hui Zhou +3 位作者 Jie Lu Yi Qu Dan Yu Yu Tong 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第1期174-179,共6页
Cerebral hypoxia or ischemia results in cell death and cerebral edema, as well as other cellular reactions such as angiogenesis and the reestablishment of functional microvasculature to promote recovery from brain inj... Cerebral hypoxia or ischemia results in cell death and cerebral edema, as well as other cellular reactions such as angiogenesis and the reestablishment of functional microvasculature to promote recovery from brain injury. Vascular endothelial growth factor is expressed in the central nervous system after hypoxic/ischemic brain injury, and is involved in the process of brain repair via the regulation of angiogenesis, neurogenesis, neurite outgrowth, and cerebral edema, which all require vascular endothelial growth factor signaling. In this review, we focus on the role of the vascular endothelial growth factor signaling pathway in the response to hypoxic/ischemic brain injury, and discuss potential therapeutic interventions. 展开更多
关键词 nerve regeneration VEGF VEGFR HIF1 PI3K/Akt pathway Akt/e NOS pathway JAK/STAT Src-SSe CKS pathway hypoxic/ischemic brain injury neural regeneration
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