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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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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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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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Ischemic postconditioning protects against ischemic brain injury by up-regulation of acid-sensing ion channel 2a 被引量:5
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作者 Wang-sheng Duanmu Liu Cao +3 位作者 Jing-yu Chen Hong-fei Ge Rong Hu Hua Feng 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第4期641-645,共5页
Ischemic postconditioning renders brain tissue tolerant to brain ischemia,thereby alleviating ischemic brain injury.However,the exact mechanism of action is still unclear.In this study,a rat model of global brain isch... Ischemic postconditioning renders brain tissue tolerant to brain ischemia,thereby alleviating ischemic brain injury.However,the exact mechanism of action is still unclear.In this study,a rat model of global brain ischemia was subjected to ischemic postconditioning treatment using the vessel occlusion method.After 2 hours of ischemia,the bilateral common carotid arteries were blocked immediately for 10 seconds and then perfused for 10 seconds.This procedure was repeated six times.Ischemic postconditioning was found to mitigate hippocampal CA1 neuronal damage in rats with brain ischemia,and up-regulate acid-sensing ion channel 2a expression at the m RNA and protein level.These findings suggest that ischemic postconditioning up-regulates acid-sensing ion channel 2a expression in the rat hippocampus after global brain ischemia,which promotes neuronal tolerance to ischemic brain injury. 展开更多
关键词 neural regeneration brain injury ischemic brain injury acid-sensing ion channels neuroprotection ischemic postconditioning neuroprotection protein expression neuronal density ischemic tolerance molecular mechanism gene expression nerve regeneration
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Mechanisms and status of research on the protective effects of traditional Chinese medicine against ischemic brain injury 被引量:1
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作者 Zhe-Tao Zhang Cheng-Yun Hu +2 位作者 Fei-Biao Dai Fei Tang Chao-Liang Tang 《Traditional Medicine Research》 2022年第1期35-43,共9页
Ischemic brain injury occurs when the metabolic needs of brain tissue cannot be met due to insufficient blood supply to the brain.It is one of the main causes of death and adult disability worldwide.The recurrence rat... Ischemic brain injury occurs when the metabolic needs of brain tissue cannot be met due to insufficient blood supply to the brain.It is one of the main causes of death and adult disability worldwide.The recurrence rate of ischemic brain injury is high.It places a heavy economic burden on families and society,and seriously affects human health and quality of life.In traditional Chinese medicine,ischemic stroke belongs to the category of“stroke”.The use of traditional Chinese medicine to treat stroke has a long history.After years of experimental research,a large amount of theoretical knowledge and practical experience have been accumulated.Promoting blood circulation and removing blood stasis is the basis of traditional Chinese medicine theory on the treatment of ischemic stroke.Commonly used single Chinese medicines include Chuangxiong(Ligusticum chuanxiong hort),Danggui(Angelica sinensis),Danshen(Salvia miltiorrhiza Bunge),Honghua(Carthamus tinctorius L.),Mudanpi(Moutan Cortex),and Huangqi(Astragali Radix).Buyang Huanwu decoction,Xinglou Chengqi decoction,Taohong Siwu decoction,and other traditional Chinese medicine prescriptions are believed to have a protective effect against brain damage caused by ischemic stroke.With the development of modern medical technology,the mechanism of traditional Chinese medicine treatments for ischemic brain injury has gradually been explored.This article reviews the mechanisms of traditional Chinese medicine’s protection against ischemic brain injury and its current clinical application. 展开更多
关键词 traditional Chinese medicine ischemic brain injury STROKE brain protection clinical application
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Repair and regeneration properties of Ginkgo biloba after ischemic brain injury 被引量:1
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作者 Aparna Raghavan Zahoor A.Shah 《Neural Regeneration Research》 SCIE CAS CSCD 2014年第11期1104-1107,共4页
The irretrievable fate of neurons rhetoric for the first half of this dominated the neuroscience century, a position that was fiercely contested and recently debunked by extensive studies carried out in the field of n... The irretrievable fate of neurons rhetoric for the first half of this dominated the neuroscience century, a position that was fiercely contested and recently debunked by extensive studies carried out in the field of neuroregeneration research. The turning point came in the year 1928, when Ramon Y. Cajal's (Lobato, 2008) work suggested that the regenerative capacity of neurons, though limited, could exist beyond their physical be- ing and depended on the environment surrounding them. That the manipulation of the restrictive environment surrounding the neuron could aid the regenerative process was conclusively established by Aguayo and colleagues (Richardson et al., 1980). Since then, various strategies have been employed to target the different phases of regeneration which include: cell-replacement and augmenting endogenous neurogenesis, the use of trophic factors, reversal of the inhibitory cues, and induction of signal- ing pathways that stimulate axon growth and guidance (Horner and Gage. 2000). 展开更多
关键词 NSCs Repair and regeneration properties of Ginkgo biloba after ischemic brain injury EGB
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Possible divergence of serum-and glucocorticoid-inducible kinase function in ischemic brain injury
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作者 Koichi Inoue 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第9期1396-1397,共2页
As recent medical progress decreases the incidence of certain diseases, ischemic brain injury remains one of the major dis- eases that threaten human lives, especially in western countries. Ischemic brain injury occur... As recent medical progress decreases the incidence of certain diseases, ischemic brain injury remains one of the major dis- eases that threaten human lives, especially in western countries. Ischemic brain injury occurs as a result of lack of oxygen and nutrients due to obstruction of blood flow in the brain, and often leads to neurological disorders such as cerebral palsy, depression, and ultimately, death. Around 800,000 Americans suffer a new or recurrent stroke, and more than 130,000 people die annually in the United States (Goldstein et al., 2011). Despite much effort in searching for an effective treatment, at most a few reagents are approved for therapeutic medication in many countries. 展开更多
关键词 SGK Possible divergence of serum-and glucocorticoid-inducible kinase function in ischemic brain injury
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Regulation of mitophagy in ischemic brain injury 被引量:13
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作者 Yang Yuan Xiangnan Zhang +1 位作者 Yanrong Zheng Zhong Chen 《Neuroscience Bulletin》 SCIE CAS CSCD 2015年第4期395-406,共12页
The selective degradation of damaged or excessive mitochondria by autophagy is termed mitophagy. Mitophagy is crucial for mitochondrial quality control and has been implicated in several neurodegenerative disorders as... The selective degradation of damaged or excessive mitochondria by autophagy is termed mitophagy. Mitophagy is crucial for mitochondrial quality control and has been implicated in several neurodegenerative disorders as well as in ischemic brain injury. Emerging evidence suggested that the role of mitophagy in cerebral ischemia may depend on different pathological processes. In particular, a neuroprotective role of mitophagy has been proposed, and the regulation of mitophagy seems to be important in cell survival. For these reasons, extensive investigations aimed to profile the mitophagy process and its underlying molecular mechanisms have been executed in recent years. In this review, we summarize the current knowledge regarding the mitophagy process and its role in cerebral ischemia, and focus on the pathological events and molecules that regulate mitophagy in ischemic brain injury. 展开更多
关键词 MITOPHAGY ischemic brain injury MITOCHONDRIA
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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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Exploring the mechanism of neuronal apoptosis and brain developmental damage in the hippocampus of hypoxicischemic neonatal rats based on BDNF/TrkB/CREB pathway
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作者 LU Tian-tian ZHANG Yao +3 位作者 LIANG Bin LIU Min CHEN Xiu-ling Jia Yan-ping 《Journal of Hainan Medical University》 2022年第18期7-12,共6页
Objective:Based on the BDNF/TrkB/CREB pathway,to explore the mechanism of neuronal apoptosis and brain developmental injury in the hippocampus of hypoxic-ischemic neonatal rats.Methods:Wistar young rats were ligated o... Objective:Based on the BDNF/TrkB/CREB pathway,to explore the mechanism of neuronal apoptosis and brain developmental injury in the hippocampus of hypoxic-ischemic neonatal rats.Methods:Wistar young rats were ligated on one side of the common carotid artery and placed in an 8%oxygen and 92%nitrogen hypoxia box for 2 h to prepare hypoxic-ischemic brain injury models.Healthy rats were used as the control group.Control group and model group were selected,with 10 rats in each group,and the learning and memory ability was tested by Y-maze;2,3,5-triphenyltetrazolium chloride(TTC)staining was used to detect brain tissue damage;Western blot was performed to determine the expression of brain-derived neurotrophic factor(BDNF),tyrosine protein kinase B(TrKB)and cAMP-response element binding protein(CREB)in hippocampal tissue.Another 15 mice in the control group and 60 mice in the model group were divided into negative control group(NC),BDNF overexpression group(LV-BDNF),TrkB overexpression group(LV-TrkB),and CREB overexpression group(LV-CREB),blank vector,BDNF,TrkB,CREB adenovirus overexpression vector was injected into the tail vein.Y-maze test for learning and memory ability;TTC staining method to detect brain tissue damage;neuronal apoptosis in the hippocampus were detected by terminal-deoxynucleoitidyl transferase mediated nick end labeling;Western blot to detect the level of neuronal apoptosis in the hippocampus.Apoptosis-related protein B-cell lymphoma-2(Bcl-2),BCL2associated X protein(Bcl-2 Assaciated X,Bax)and nuclear factor kappaB(NFκB)expression.Results:The learning and memory ability of the young mice in the model group was significantly reduced,the brain infarct volume was significantly increased,the expressions of BDNF and TrkB proteins in the hippocampus were significantly increased,and the expression of CREB proteins was significantly decreased;After overexpression of BDNF and TrkB CREB,in the LVBDNF,LVTrkB,and LVCREB group,the learning and memory ability of young mice were significantly improved,the brain infarct volume were significantly reduced,the hippocampal neuronal apoptosis were significantly reduced,The protein expression of Bax and NFκB were significantly decreased and the protein expression of Bcl2 were significantly enhanced.Conclusion:The expression of BDNF/TrkB/CREB is abnormal in HIBI model young mice.Overexpression of BDNF/TrkB/CREB can improve the learning and memory ability of young mice,repair brain tissue damage,and inhibit neuronal apoptosis.Therefore,the mechanism of HIBI may be related to BDNF/TrkB/CREB pathways. 展开更多
关键词 Hypoxic‑ischemic brain injury Neuronal apoptosis BDNF TRKB CREB
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The superiority and feasibility of 2,3,5-triphenyltetrazolium chloride-stained brain tissues for molecular biology experiments based on microglial properties
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作者 Yajuan Wang Qingrong Zhang +2 位作者 Shuchi Zhang Jiangtao Qi Li Li 《Animal Models and Experimental Medicine》 CAS CSCD 2023年第2期111-119,共9页
Background:TTC(2,3,5-triphenyltetrazolium chloride)staining is the most commonly used method in identifying and assessing cerebral infarct volumes in the transient middle cerebral artery occlusion model.Given that mic... Background:TTC(2,3,5-triphenyltetrazolium chloride)staining is the most commonly used method in identifying and assessing cerebral infarct volumes in the transient middle cerebral artery occlusion model.Given that microglia exhibit different morphologies in different regions after ischemic stroke,we demonstrate the superiority and necessity of using TTC-stained brain tissue to analyze the expression of various proteins or genes in different regions based on microglia character.Methods:We compared brain tissue(left for 10 min on ice)from the improved TTC staining method with penumbra from the traditional sampling method.We identified the feasibility and necessity of the improved staining method using real time(RT)-PCR,Western blot,and immunofluorescence analysis.Results:There was no protein and RNA degradation in the TTC-stained brain tissue group.However,the TREM2 specifically expressed on the microglia showed a significant difference between two groups in the penumbra region.Conclusions:TTC-stained brain tissue can be used for molecular biology experiments without any restrictions.In addition,TTC-stained brain tissue shows greater superiority due to its precise positioning. 展开更多
关键词 ischemic brain injury MICROGLIA transient middle cerebral artery occlusion TTC staining
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Effects of Remifentanil Pretreatment on Inflammatory Response in Rats with Acute Cerebral Ischemia Injury
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作者 Jingfeng ZHOU Xianjing ZENG +2 位作者 Shu LIU Jinghua YUAN Fan XIAO 《Medicinal Plant》 2023年第6期56-59,共4页
[Objectives]This study was conducted to investigate the effects of remifentanil pretreatment on inflammatory factors in rats with acute cerebral ischemia.[Methods]Sixty SD rats were randomly divided into the normal co... [Objectives]This study was conducted to investigate the effects of remifentanil pretreatment on inflammatory factors in rats with acute cerebral ischemia.[Methods]Sixty SD rats were randomly divided into the normal control group,sham operation group,ischemic brain injury group,and remifentanil pretreatment group.Except the normal control group,each group was divided into three subgroups(six in each group)according to the sampling time points of 6,12 and 24 h after execution.After modeling,the rats were scored for neurological deficit,and observed for pathological changes of neurons in the brain tissue by HE staining and the brain infarct volume by TTC staining,and the expression levels of TNF-α,IL-6 and IL-8 were detected by RT-PCR.[Results]HE staining:No significant changes were observed in the pathological morphology of the brain tissue in the blank group and sham operation group;and the neuronal structure of rats in the acute cerebral ischemia group was obviously damaged,and the neuronal damage in the remifentanil pretreatment group was less than that in the acute cerebral ischemia group at each time point.TTC staining:The gray brain infarct area in the remifentanil pretreatment group was significantly smaller than that in the cerebral ischemia group(P<0.05).RT-PCR detection results:The expression levels of TNF-α,IL-6 and IL-8 in the blank group and sham surgery group did not show significant changes at different times(P>0.05);and compared with the cerebral ischemia group,the expression levels of TNF-α,IL-6,and IL-8 in the remifentanil pretreatment group were significantly reduced at all time points(P<0.05).[Conclusions]Remifentanil pretreatment could protect the brain by reducing the expression of inflammatory factors after cerebral ischemia injury. 展开更多
关键词 REMIFENTANIL Acute ischemic brain injury Tumor necrosis factor INTERLEUKIN-6 INTERLEUKIN-8
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The role of glycogen synthase kinase 3 beta in brain injury induced by myocardial ischemia/reperfusion injury in a rat model of diabetes mellitus 被引量:8
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作者 Bo Zhao Wen-wei Gao +5 位作者 Ya-jing Liu Meng Jiang Lian Liu Quan Yuan Jia-bao Hou Zhong-yuan Xia 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第10期1632-1639,共8页
Myocardial ischemia/reperfusion injury can lead to severe brain injury.Glycogen synthase kinase 3 beta is known to be involved in myocardial ischemia/reperfusion injury and diabetes mellitus.However,the precise role o... Myocardial ischemia/reperfusion injury can lead to severe brain injury.Glycogen synthase kinase 3 beta is known to be involved in myocardial ischemia/reperfusion injury and diabetes mellitus.However,the precise role of glycogen synthase kinase 3 beta in myocardial ischemia/reperfusion injury-induced brain injury is unclear.In this study,we observed the effects of glycogen synthase kinase 3 beta on brain injury induced by myocardial ischemia/reperfusion injury in diabetic rats.Rat models of diabetes mellitus were generated via intraperitoneal injection of streptozotocin.Models of myocardial ischemia/reperfusion injury were generated by occluding the anterior descending branch of the left coronary artery.Post-conditioning comprised three cycles of ischemia/reperfusion.Immunohistochemical staining and western blot assays demonstrated that after 48 hours of reperfusion,the structure of the brain was seriously damaged in the experimental rats compared with normal controls.Expression of Bax,interleukin-6,interleukin-8,terminal deoxynucleotidyl transferase d UTP nick end labeling,and cleaved caspase-3 in the brain was significantly increased,while expression of Bcl-2,interleukin-10,and phospho-glycogen synthase kinase 3 beta was decreased.Diabetes mellitus can aggravate inflammatory reactions and apoptosis.Ischemic post-conditioning with glycogen synthase kinase 3 beta inhibitor lithium chloride can effectively reverse these changes.Our results showed that myocardial ischemic post-conditioning attenuated myocardial ischemia/reperfusion injury-induced brain injury by activating glycogen synthase kinase 3 beta.According to these results,glycogen synthase kinase 3 beta appears to be an important factor in brain injury induced by myocardial ischemia/reperfusion injury. 展开更多
关键词 nerve regeneration myocardial ischemia/reperfusion injury brain injury glycogen synthase kinase 3 beta ischemic post-conditioning diabetes mellitus neural regeneration
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Inhibition of cerebral ischemia/reperfusion injuryinduced apoptosis:nicotiflorin and JAK2/STAT3 pathway 被引量:39
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作者 Guang-qiang Hu Xi Du +3 位作者 Yong-jie Li Xiao-qing Gao Bi-qiong Chen Lu Yu 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第1期96-102,共7页
Nicotiflorin is a flavonoid extracted from Carthamus tinctorius.Previous studies have shown its cerebral protective effect,but the mechanism is undefined.In this study,we aimed to determine whether nicotiflorin protec... Nicotiflorin is a flavonoid extracted from Carthamus tinctorius.Previous studies have shown its cerebral protective effect,but the mechanism is undefined.In this study,we aimed to determine whether nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis through the JAK2/STAT3 pathway.The cerebral ischemia/reperfusion injury model was established by middle cerebral artery occlusion/reperfusion.Nicotiflorin(10 mg/kg) was administered by tail vein injection.Cell apoptosis in the ischemic cerebral cortex was examined by hematoxylin-eosin staining and terminal deoxynucleotidyl transferase d UTP nick end labeling assay.Bcl-2 and Bax expression levels in ischemic cerebral cortex were examined by immunohistochemial staining.Additionally,p-JAK2,p-STAT3,Bcl-2,Bax,and caspase-3 levels in ischemic cerebral cortex were examined by western blot assay.Nicotiflorin altered the shape and structure of injured neurons,decreased the number of apoptotic cells,down-regulates expression of p-JAK2,p-STAT3,caspase-3,and Bax,decreased Bax immunoredactivity,and increased Bcl-2 protein expression and immunoreactivity.These results suggest that nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis via the JAK2/STAT3 pathway. 展开更多
关键词 nerve regeneration brain injury nicotiflorin ischemic stroke cerebral ischemia/reperfusion injury treatment cell apoptosis terminal deoxynucleotidyl transferase dUTP nick end labeling JAK2/STAT3 pathway Bcl-2 Bax caspase-3 neural regeneration
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Simple diffusion delivery via brain interstitial route for the treatment of cerebral ischemia 被引量:24
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作者 HAN HongBin XIA ZuoLi +2 位作者 CHEN He HOU Chao LI WeiBo 《Science China(Life Sciences)》 SCIE CAS 2011年第3期235-239,共5页
Delivering pharmacologic agents directly into the brain has been proposed as a means of bypassing the blood brain barrier.However,despite 16 years of research on a number of central nervous system disorders,an effecti... Delivering pharmacologic agents directly into the brain has been proposed as a means of bypassing the blood brain barrier.However,despite 16 years of research on a number of central nervous system disorders,an effective treatment using this strategy has only been observed in the brain tumor glioblastoma multiforme.Within this study we propose a novel system for delivering drugs into the brain named the simple diffusion (SDD) system.To validate this technique,rats were subjected to a single intracranial (at the caudate nucleus),or intraperitoneal injection,of the compound citicoline,followed two hours later by a permanent middle cerebral artery occlusion (pMCAO).Results showed that 12 h after pMCAO,with 0.0025 g kg-1 citicoline,an infarct volume 1/6 the size of the intraperitoneal group was achieved with a dose 1/800 of that required for the intraperitoneal group.These results suggest that given the appropriate injection point,through SDD a pharmacologically effective concentration of citicoline can be administered. 展开更多
关键词 permanent middle cerebral artery occlusion animal model brain ischemic injury citicoline therapy MRI NEUROPROTECTION
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Research advances on antioxidation,neuroprotection,and molecular mechanisms of Lycium barbarum polysaccharides 被引量:2
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作者 Cheng Wang Liangxing Zhou +9 位作者 Mei Mo Xianglin Kong Zhengbin Chai Lei Deng Junli Zhang Kuan Cao Chuanfei Wei Li Xu Juanli Chen Fabin Han 《Brain Science Advances》 2021年第4期207-219,共13页
Lycium barbarum polysaccharides(LBPs)are the major polysaccharides extracted from L.barbarum,which is used in traditional Chinese medicine(TCM)for treating diseases.Studies have shown that LBPs have important biologic... Lycium barbarum polysaccharides(LBPs)are the major polysaccharides extracted from L.barbarum,which is used in traditional Chinese medicine(TCM)for treating diseases.Studies have shown that LBPs have important biological activities,such as antioxidation,anti-aging,neuroprotection,immune regulation.LBPs inhibit oxidative stress,improve neurodegeneration and stroke-induced neural injury,increase proliferation and differentiation of neural stem cell,and promote neural regeneration.Here we have reviewed latest advances in the biomedical activities of LBPs and improved methods for the isolation,extraction,and purification of LBPs.Then,new discoveries to decrease oxidative stress and cellular apoptosis,inhibit aging progress,and improve neural repair in neurodegeneration and ischemic brain injury have been discussed in detail through in vitro cell culture and in vivo animal studies.Importantly,the molecular mechanisms of LBPs in playing neuroprotective roles are further explored.Lastly,we discuss the perspective of LBPs as biomedical compounds in TCM and modern medicine and provide the experimental and theoretical evidence to use LBPs for the treatment of aging-related neurological diseases and stroke-induced neural injuries. 展开更多
关键词 Lycium barbarum polysaccharide oxidative stress NEUROPROTECTION neurodegenerative disease ischemic brain injury neural stem cell
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Advances in Studies on Pharmacological Functions of Ligustilide and their Mechanisms 被引量:1
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作者 Jin-ying YANG Hu-hu CHEN +4 位作者 Jiang WU Su-xiao GONG Chang-qing CHEN Tie-jun ZHANG Min-jie WANG 《Chinese Herbal Medicines》 CAS 2012年第1期26-32,共7页
The article reviewed the research progress of ligustilide in recent years and elaborated its pharmacological functions and mechanisms in detail, especially in ischemic brain injury. Its mechanism includes reducing cer... The article reviewed the research progress of ligustilide in recent years and elaborated its pharmacological functions and mechanisms in detail, especially in ischemic brain injury. Its mechanism includes reducing cerebral infarct volumes and improving neurobehavioral deficits, anti-oxidant and anti-apoptosis, antithrombotic activity, calcium channel blockers function, and effect on erythropoietin. Other pharmacological effects of ligustilide including inhibiting vascular smooth muscle cell proliferation, anti-inflammatory and analgesic effects, effects on LPS-induced endotoxic shock, inhibiting constriction effect, suppression of the central nervous system, and ameliorating the memory impairment induced by scopolamine and so on, are also introduced. Ligustilide has potential pharmacological value, which provides a reference for its further research and development. 展开更多
关键词 cerebral infarct ischemic brain injury LIGUSTILIDE neurobehavioral deficit pharmacological function and mechanism
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