期刊文献+
共找到63,925篇文章
< 1 2 250 >
每页显示 20 50 100
Inhibiting endogenous tissue plasminogen activator enhanced neuronal apoptosis and axonal injury after traumatic brain injury 预览
1
作者 Jun-Jie Zhao Zun-Wei Liu +4 位作者 Bo Wang Ting-Qin Huang Dan Guo Yong-Lin Zhao Jin-Ning Song 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第4期667-675,共9页
Tissue plasminogen activator is usually used for the treatment of acute ischemic stroke,but the role of endogenous tissue plasminogen activator in traumatic brain injury has been rarely reported.A rat model of traumat... Tissue plasminogen activator is usually used for the treatment of acute ischemic stroke,but the role of endogenous tissue plasminogen activator in traumatic brain injury has been rarely reported.A rat model of traumatic brain injury was established by weight-drop method.The tissue plasminogen activator inhibitor neuroserpin(5μL,0.25 mg/mL)was injected into the lateral ventricle.Neurological function was assessed by neurological severity score.Neuronal and axonal injuries were assessed by hematoxylin-eosin staining and Bielschowsky silver staining.Protein level of endogenous tissue plasminogen activator was analyzed by western blot assay.Apoptotic marker cleaved caspase-3,neuronal marker neurofilament light chain,astrocyte marker glial fibrillary acidic protein and microglial marker Iba-1 were analyzed by immunohistochemical staining.Apoptotic cell types were detected by immunofluorescence double labeling.Apoptotic cells in the damaged cortex were detected by terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP-biotin nick-end labeling staining.Degenerating neurons in the damaged cortex were detected by Fluoro-Jade B staining.Expression of tissue plasminogen activator was increased at 6 hours,and peaked at 3 days after traumatic brain injury.Neuronal apoptosis and axonal injury were detected after traumatic brain injury.Moreover,neuroserpin enhanced neuronal apoptosis,neuronal injury and axonal injury,and activated microglia and astrocytes.Neuroserpin further deteriorated neurobehavioral function in rats with traumatic brain injury.Our findings confirm that inhibition of endogenous tissue plasminogen activator aggravates neuronal apoptosis and axonal injury after traumatic brain injury,and activates microglia and astrocytes.This study was approved by the Biomedical Ethics Committee of Animal Experiments of Shaanxi Province of China in June 2015. 展开更多
关键词 apoptosis ASTROCYTES AXONAL INJURY inflammation microglia nerve REGENERATION neural REGENERATION neuronal INJURY neurons NEUROSERPIN tissue PLASMINOGEN activator traumatic brain INJURY
在线阅读 下载PDF
Optimal concentration of necrostatin-1 for protecting against hippocampal neuronal damage in mice with status epilepticus 预览
2
作者 Dong-Qi Lin Xin-Ying Cai +2 位作者 Chun-Hua Wang Bin Yang Ri-Sheng Liang 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第5期936-943,共8页
Hippocampal neurons undergo various forms of cell death after status epilepticus.Necrostatin-1 specifically inhibits necroptosis mediated by receptor interacting protein kinase 1 (RIP1) and RIP3 receptors.However,ther... Hippocampal neurons undergo various forms of cell death after status epilepticus.Necrostatin-1 specifically inhibits necroptosis mediated by receptor interacting protein kinase 1 (RIP1) and RIP3 receptors.However,there are no reports of necroptosis in mouse models of status epilepticus.Therefore,in this study,we investigated the effects of necrostatin-1 on hippocampal neurons in mice with status epilepticus,and,furthermore,we tested different amounts of the compound to identify the optimal concentration for inhibiting necroptosis and apoptosis.A mouse model of status epilepticus was produced by intraperitoneal injection of kainic acid,12 mg/kg.Different concentrations of necrostatin- 1 (10,20,40,and 80 μM) were administered into the lateral ventricle 15 minutes before kainic acid injection.Hippocampal damage was assessed by hematoxylin-eosin staining 24 hours after the model was successfully produced.Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining,western blot assay and immunohistochemistry were used to evaluate the expression of apoptosis-related and necroptosis-related proteins.Necrostatin-1 alleviated damage to hippocampal tissue in the mouse model of epilepsy.The 40 μM concentration of necrostatin-1 significantly decreased the number of apoptotic cells in the hippocampal CA1 region.Furthermore,necrostatin-1 significantly downregulated necroptosis-related proteins (MLKL,RIP1,and RIP3) and apoptosis-related proteins (cleaved-Caspase-3,Bax),and it upregulated the expression of anti-apoptotic protein Bcl-2.Taken together,our findings show that necrostatin-1 effectively inhibits necroptosis and apoptosis in mice with status epilepticus,with the 40 μM concentration of the compound having an optimal effect.The experiments were approved by the Animal Ethics Committee of Fujian Medical University,China (approval No.2016-032) on November 9,2016. 展开更多
关键词 apoptosis Bax Bcl-2 cleaved-Caspase-3 EPILEPSY HIPPOCAMPAL NEURON MLKL NECROPTOSIS necrostatin-1 NERVE REGENERATION neural REGENERATION RIP1 RIP3
在线阅读 下载PDF
Ligustilide protects PC12 cells from oxygen-glucose deprivation/reoxygenation-induced apoptosis via the LKB1-AMPK-mTOR signaling pathway 预览
3
作者 Dan-Yang Zhao Dong-Dong Yu +1 位作者 Li Ren Guo-Rong Bi 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第3期473-481,共9页
Autophagy has been shown to have a protective effect against brain damage.Ligustilide(LIG)is a bioactive substance isolated from Ligusticum chuanxiong,a traditional Chinese medicine.LIG has a neuroprotective effect;ho... Autophagy has been shown to have a protective effect against brain damage.Ligustilide(LIG)is a bioactive substance isolated from Ligusticum chuanxiong,a traditional Chinese medicine.LIG has a neuroprotective effect;however,it is unclear whether this neuroprotective effect involves autophagy.In this study,PC12 cells were treated with 1×10^-5–1×10^-9 M LIG for 0,3,12 or 24 hours,and cell proliferation was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium(MTS)assay.Treatment with 1×10^-6 M LIG for 3 hours had the greatest effect on cell proliferation,and was therefore used for subsequent experiments.PC12 cells were pre-treated with 1×10^-6 M LIG for 3 hours,cultured in 95%N2/5%CO2 in Dulbecco’s modified Eagle’s medium without glucose or serum for 4 hours,and then cultured normally for 16 hours,to simulate oxygen-glucose deprivation/reoxygenation(OGD/R).Cell proliferation was assessed with the MTS assay.Apoptosis was detected by flow cytometry.The expression levels of apoptosis-related proteins,Bcl-2 and Bax,autophagy-related proteins,Beclin 1 and microtubule-associated protein l light chain 3B(LC3-II),and liver kinase B1(LKB1)-5′-adenosine monophosphate-activated protein kinase(AMPK)-mammalian target of rapamycin(mTOR)signaling pathway-related proteins were assessed by western blot assay.Immunofluorescence staining was used to detect LC3-II expression.Autophagosome formation was observed by electron microscopy.LIG significantly decreased apoptosis,increased Bcl-2,Beclin 1 and LC3-II expression,decreased Bax expression,increased LC3-II immunoreactivity and the number of autophagosomes,and activated the LKB1-AMPK-mTOR signaling pathway in PC12 cells exposed to OGD/R.The addition of the autophagy inhibitor 3-methyladenine or dorsomorphin before OGD/R attenuated the activation of the LKB1-AMPK-mTOR signaling pathway in cells treated with LIG.Taken together,our findings show that LIG promotes autophagy and protects PC12 cells from apoptosis induced by 展开更多
关键词 AMPK apoptosis autophagy Bax Bcl-2 BECLIN 1 LC3-II LIGUSTILIDE mTOR PC12 cells
在线阅读 下载PDF
Time course analysis of sensory axon regeneration in vivo by directly tracing regenerating axons 预览
4
作者 Yan Gao Yi-Wen Hu +3 位作者 Run-Shan Duan Shu-Guang Yang Feng-Quan Zhou Rui-Ying Wang 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第6期1160-1165,共6页
Most current studies quantify axon regeneration by immunostaining regeneration-associated proteins,representing indirect measurement of axon lengths from both sensory neurons in the dorsal root ganglia and motor neuro... Most current studies quantify axon regeneration by immunostaining regeneration-associated proteins,representing indirect measurement of axon lengths from both sensory neurons in the dorsal root ganglia and motor neurons in the spinal cord.Our recently developed method of in vivo electroporation of plasmid DNA encoding for enhanced green fluorescent protein into adult sensory neurons in the dorsal root ganglia provides a way to directly and specifically measure regenerating sensory axon lengths in whole-mount nerves.A mouse model of sciatic nerve compression was established by squeezing the sciatic nerve with tweezers.Plasmid DNA carrying enhanced green fluorescent protein was transfected by ipsilateral dorsal root ganglion electroporation 2 or 3 days before injury.Fluorescence distribution of dorsal root or sciatic nerve was observed by confocal microscopy.At 12 and 18 hours,and 1,2,3,4,5,and 6 days of injury,lengths of regenerated axons after sciatic nerve compression were measured using green fluorescence images.Apoptosis-related protein caspase-3 expression in dorsal root ganglia was determined by western blot assay.We found that in vivo electroporation did not affect caspase-3 expression in dorsal root ganglia.Dorsal root ganglia and sciatic nerves were successfully removed and subjected to a rapid tissue clearing technique.Neuronal soma in dorsal root ganglia expressing enhanced green fluorescent protein or fluorescent dye-labeled microRNAs were imaged after tissue clearing.The results facilitate direct time course analysis of peripheral nerve axon regeneration.This study was approved by the Institutional Animal Care and Use Committee of Guilin Medical University,China(approval No.GLMC201503010)on March 7,2014. 展开更多
关键词 axon regeneration cell apoptosis dorsal root ganglion in vivo electroporation micro RNAs peripheral nervous system sciatic nerve tissue clearing
在线阅读 下载PDF
Regulation of apoptosis in the ischemic penumbra in the first day post-stroke 预览
5
作者 Anatoly B. Uzdensky 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期253-254,共2页
Stroke is one of leading causes of human disability and death. More than 17 million stroke incidences occur in the world each year. In ischemic stroke (70-80% of all strokes) cerebral vessel occlusion quickly, for few... Stroke is one of leading causes of human disability and death. More than 17 million stroke incidences occur in the world each year. In ischemic stroke (70-80% of all strokes) cerebral vessel occlusion quickly, for few minutes causes oxygen and glucose depletion, ATP deficit, and tissue infarction. 展开更多
关键词 HUMAN DISABILITY APOPTOSIS depletion
在线阅读 下载PDF
小檗碱干预2型糖尿病模型大鼠脑缺血再灌注损伤 预览
6
作者 符芸瑜 邱晓堂 +3 位作者 杨文奎 莫世安 吴小翠 吴英萍 《中国组织工程研究》 CAS 北大核心 2020年第2期230-235,共6页
背景:既往研究提示小檗碱可减轻脑缺血再灌注损伤。目的:探讨小檗碱对2型糖尿病大鼠脑缺血再灌注损伤的影响及其分子机制。方法:实验方案经海南省中医院伦理委员会批准。用低剂量链脲佐菌素30 mg/kg每隔1 d大鼠腹腔注射2次,处理8周建立... 背景:既往研究提示小檗碱可减轻脑缺血再灌注损伤。目的:探讨小檗碱对2型糖尿病大鼠脑缺血再灌注损伤的影响及其分子机制。方法:实验方案经海南省中医院伦理委员会批准。用低剂量链脲佐菌素30 mg/kg每隔1 d大鼠腹腔注射2次,处理8周建立2型糖尿病模型,选取平均血糖≥11.1 mmol/L造模成功的雄性SD大鼠90只,随机分为对照组、缺血/再灌注组和缺血/再灌注+小檗碱组,每组30只。对照组和缺血/再灌注组大鼠经生理盐水灌胃,缺血/再灌注+小檗碱组用小檗碱200 mg/(kg·d)灌胃,处理7 d后,后2组采用大脑中动脉阻断2 h,再灌注12 h建立大脑中动脉缺血再灌注模型。苏木精-伊红染色和透射电镜观察脑梗死体积;采用ELISA检测梗死区超氧化物歧化酶、丙二醛和一氧化氮水平;采用TUNEL法检测脑细胞凋亡情况;Westernblot检测PI3K、Akt和磷酸化Akt(p-Akt)蛋白的表达。结果与结论:①与缺血/再灌注组比较,缺血/再灌注+小檗碱组脑梗死体积明显减少(P<0.05),超氧化物歧化酶水平明显升高,丙二醛和一氧化氮的表达明显降低;②与缺血/再灌注组比较,缺血/再灌注+小檗碱组脑梗死区细胞凋亡减少,Bcl-2表达增加,cleaved-Caspase3和Bax表达降低;③与缺血/再灌注组相比,小檗碱可使缺血/再灌注+小檗碱组PI3K和p-Akt的表达水平明显上调;④结果说明,小檗碱可通过激活PI3K-Akt信号通路,在2型糖尿病大鼠脑缺血模型中发挥抗凋亡作用,减轻脑缺血/再灌注损伤。 展开更多
关键词 缺血再灌注 2型糖尿病 小檗碱 凋亡 PI3K-AKT
在线阅读 下载PDF
tRNA cleavage:a new insight 预览
7
作者 Sherif Rashad Kuniyasu Niizuma Teiji Tominaga 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第1期47-52,共6页
Over the past decades,tRNA was found to be a rich hub of RNA modifications such as 1-methyladenosine and 5-methycytosine modifications and others,holding more than half of all modifications occurring in RNA molecules.... Over the past decades,tRNA was found to be a rich hub of RNA modifications such as 1-methyladenosine and 5-methycytosine modifications and others,holding more than half of all modifications occurring in RNA molecules.Moreover,tRNA was discovered to be a source of various small noncoding RNA species,such as the stress induced angiogenin cleaved tRNA halves(tiRNA)or the miRNA like tRNA derived fragments.tRNA cleavage under stress was fist discovered in bacteria and later was found to be conserved across different species,including mammals.Under cellular stress conditions,tRNA undergoes conformational changes and angiogenin cleaves it into 3′and 5′halves.5′tiRNA halves were shown to repress protein translations.tRNA cleavage is thought of to be a cytoprotective mechanism by which cells evade apoptosis,however some data hints to the opposite;that tiRNA are cytotoxic or at least related to apoptosis initiation.tRNA cleavage also was shown to be affected by tRNA modifications via different enzymes in the cytosol and mitochondria.In this review,we will highlight the biology of tRNA cleavage,show the evidence of it being cytoprotective or a marker of cell death and shed a light on its role in disease models and human diseases as well as possible future directions in this field of RNA research. 展开更多
关键词 ANGIOGENIN apoptosis cell STRESS RNA modification STRESS GRANULES stroke tiRNA translation REPRESSION TRNA TRNA CLEAVAGE
在线阅读 下载PDF
Achyranthes bidentata polypeptides prevent apoptosis by inhibiting the glutamate current in cultured hippocampal neurons 预览
8
作者 Rong-Lu Pan Wen-Qing Hu +3 位作者 Jie Pan Li Huang Cheng-Cheng Luan Hong-Mei Shen 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第6期1086-1093,共8页
Glutamate-induced excitotoxicity plays a critical role in the neurological impairment caused by middle cerebral artery occlusion.Achyranthes bidentata polypeptides have been shown to protect against neurological funct... Glutamate-induced excitotoxicity plays a critical role in the neurological impairment caused by middle cerebral artery occlusion.Achyranthes bidentata polypeptides have been shown to protect against neurological functional damage caused by middle cerebral artery occlusion,but the underlying neuroprotective mechanisms and the relationship to glutamate-induced excitotoxicity remain unclear.Therefore,in the current study,we investigated the protective effects of Achyranthes bidentata polypeptides against glutamate-induced excitotoxicity in cultured hippocampal neurons.Hippocampal neurons were treated with Mg^2+-free extracellular solution containing glutamate(300μM)for 3 hours as a model of glutamate-mediated excitotoxicity(glutamate group).In the normal group,hippocampal neurons were incubated in Mg^2+-free extracellular solution.In the Achyranthes bidentata polypeptide group,hippocampal neurons were incubated in Mg^2+-free extracellular solution containing glutamate(300μM)and Achyranthes bidentata polypeptide at different concentrations.At 24 hours after exposure to the agents,3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and Hoechst 33258 staining were used to assess neuronal viability and nuclear m'orphology,respectively.Caspase-3 expression and activity were evaluated using western blot assay and colorimetric enzymatic assay,respectively.At various time points after glutamate treatment,reactive oxygen species in cells were detected by H2 DCF-DA,and mitochondrial membrane potential was detected by rhodamine 123 staining.To examine the effect of Achyranthes bidentata polypeptides on glutamate receptors,electrophysiological recording was used to measure the glutamate-induced inward current in cultured hippocampal neurons.Achyranthes bidentata polypeptide decreased the percentage of apoptotic cells and reduced the changes in caspase-3 expression and activity induced by glutamate.In addition,Achyranthes bidentata polypeptide attenuated the amplitude of the glutamate-induced current.Furthermore 展开更多
关键词 Achyranthes bidentata polypeptides APOPTOSIS caspase-3 EXCITOTOXICITY glutamate receptors mitochondrial dysfunction mitochondrial membrane potential NEUROPROTECTION reactive oxygen species STAUROSPORINE
在线阅读 下载PDF
Selective brain hypothermia-induced neuroprotection against focal cerebral ischemia/reperfusion injury is associated with Fis1 inhibition 预览
9
作者 Ya-Nan Tang Gao-Feng Zhang +6 位作者 Huai-Long Chen Xiao-Peng Sun Wei-Wei Qin Fei Shi Li-Xin Sun Xiao-Na Xu Ming-Shan Wang 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第5期903-911,共9页
Selective brain hypothermia is considered an effective treatment for neuronal injury after stroke,and avoids the complications of general hypothermia.However,the mechanisms by which selective brain hypothermia affects... Selective brain hypothermia is considered an effective treatment for neuronal injury after stroke,and avoids the complications of general hypothermia.However,the mechanisms by which selective brain hypothermia affects mitochondrial fission remain unknown.In this study,we investigated the effect of selective brain hypothermia on the expression of fission 1 (Fis1) protein,a key factor in the mitochondrial fission system,during focal cerebral ischemia/reperfusion injury.Sprague-Dawley rats were divided into four groups.In the sham group,the carotid arteries were exposed only.In the other three groups,middle cerebral artery occlusion was performed using the intraluminal filament technique.After 2 hours of occlusion,the filament was slowly removed to allow blood reperfusion in the ischemia/reperfusion group.Saline,at 4℃ and 37℃,were perfused through the carotid artery in the hypothermia and normothermia groups,respectively,followed by restoration of blood flow.Neurological function was assessed with the Zea Longa 5-point scoring method.Cerebral infarct volume was assessed by 2,3,5-triphenyltetrazolium chloride staining,and apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining.Fis1 and cytosolic cytochrome c levels were assessed by western blot assay.Fis1 mRNA expression was assessed by quantitative reverse transcription-polymerase chain reaction.Mitochondrial ultrastructure was evaluated by transmission electron microscopy.Compared with the sham group,apoptosis,Fis1 protein and mRNA expression and cytosolic cytochrome c levels in the cortical ischemic penumbra and cerebral infarct volume were increased after reperfusion in the other three groups.These changes caused by cerebral ischemia/reperfusion were inhibited in the hypothermia group compared with the normothermia group.These findings show that selective brain hypothermia inhibits Fis1 expression and reduces apoptosis,thereby ameliorating focal cerebral ischemia/reperfusion injury in rats.Experiments were auth 展开更多
关键词 apoptosis Fis1 HYPOTHERMIA ISCHEMIA/REPERFUSION injury mitochondria MITOCHONDRIAL fission MITOCHONDRIAL ultrastructure NEUROPROTECTION SELECTIVE BRAIN HYPOTHERMIA stroke
在线阅读 下载PDF
Transfer of mitochondria from mesenchymal stem cells derived from induced pluripotent stem cells attenuates hypoxia-ischemia-induced mitochondrial dysfunction in PC12 cells 预览
10
作者 Yan Yang Gen Ye +5 位作者 Yue-Lin Zhang Hai-Wei He Bao-Qi Yu Yi-Mei Hong Wei You Xin Li 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第3期464-472,共9页
Mitochondrial dysfunction in neurons has been implicated in hypoxia-ischemia-induced brain injury.Although mesenchymal stem cell therapy has emerged as a novel treatment for this pathology,the mechanisms are not fully... Mitochondrial dysfunction in neurons has been implicated in hypoxia-ischemia-induced brain injury.Although mesenchymal stem cell therapy has emerged as a novel treatment for this pathology,the mechanisms are not fully understood.To address this issue,we first co-cultured 1.5×10^5 PC12 cells with mesenchymal stem cells that were derived from induced pluripotent stem cells at a ratio of 1:1,and then intervened with cobalt chloride(CoCl2)for 24 hours.Reactive oxygen species in PC12 cells was measured by Mito-sox.Mitochondrial membrane potential(ΔΨm)in PC12 cells was determined by JC-1 staining.Apoptosis of PC12 cells was detected by terminal deoxynucleotidal transferase-mediated dUTP nick end-labeling staining.Mitochondrial morphology in PC12 cells was examined by transmission electron microscopy.Transfer of mitochondria from the mesenchymal stem cells derived from induced pluripotent stem cells to damaged PC12 cells was measured by flow cytometry.Mesenchymal stem cells were induced from pluripotent stem cells by lentivirus infection containing green fluorescent protein in mitochondria.Then they were co-cultured with PC12 cells in Transwell chambers and treated with CoCl2 for 24 hours to detect adenosine triphosphate level in PC12 cells.CoCl2-induced PC12 cell damage was dose-dependent.Co-culture with mesenchymal stem cells significantly reduced apoptosis and restoredΔΨm in the injured PC12 cells under CoCl2 challenge.Co-culture with mesenchymal stem cells ameliorated mitochondrial swelling,the disappearance of cristae,and chromatin margination in the injured PC12 cells.After direct co-culture,mitochondrial transfer from the mesenchymal stem cells stem cells to PC12 cells was detected via formed tunneling nanotubes between these two types of cells.The transfer efficiency was greatly enhanced in the presence of CoCl2.More importantly,inhibition of tunneling nanotubes partially abrogated the beneficial effects of mesenchymal stem cells on CoCl2-induced PC12 cell injury.Mesenchymal stem cells reduced CoCl2-induced 展开更多
关键词 apoptosis brain injury HYPOXIA-ISCHEMIA INDUCED pluripotent STEM CELLS mesenchymal STEM CELLS MITOCHONDRIAL membrane potential MITOCHONDRIAL TRANSFER PC12 CELLS tunneling nanotubes
在线阅读 下载PDF
腰椎肥厚黄韧带中细胞凋亡及凋亡因子caspase-3、fas、p53的表达 预览
11
作者 张方新 康朋 +4 位作者 王起腾 张晓 刘伟 杨红涛 艾尔肯•阿木冬 《中国组织工程研究》 CAS 北大核心 2020年第8期1195-1199,共5页
背景:腰椎管狭窄症是造成老年人步态紊乱和腰腿痛的关键原因之一,黄韧带肥厚是导致腰椎管狭窄症的主要病理机制,目前关于黄韧带的影像学及病理研究较多,关于细胞凋亡的研究较少。目的:检测肥厚黄韧带组织中的细胞凋亡率及凋亡因子caspas... 背景:腰椎管狭窄症是造成老年人步态紊乱和腰腿痛的关键原因之一,黄韧带肥厚是导致腰椎管狭窄症的主要病理机制,目前关于黄韧带的影像学及病理研究较多,关于细胞凋亡的研究较少。目的:检测肥厚黄韧带组织中的细胞凋亡率及凋亡因子caspase-3、fas、p53的表达,为深入了解黄韧带退变的机制提供实验依据。方法:实验组50个经MRI及术后测量证实肥厚黄韧带标本(L 2-S 1)来自50例腰椎管狭窄症行后路减压手术自愿捐赠的患者,男22例,女28例,年龄32-74岁,平均54.46岁;对照组30个经MRI及术后测量证实非肥厚黄韧带标本(L 2-S 1)来自30例腰椎间盘突出症行手术及腰椎爆裂骨折行手术患者,男19例,女11例,年龄19-67岁,平均47.27岁。采用TUNEL染色法检测黄韧带中的凋亡细胞率,用SP免疫组织化学法检测caspase-3、fas、p53的表达。研究通过了新疆医科大学第六附属医院伦理委员会批准,伦理编号为LFYLLSJ2016007。结果与结论:①TUNEL染色示实验组的平均凋亡细胞率高于对照组[(37.80±3.04)%,(13.18±1.34)%,t=41.83,P<0.001];②SP免疫组织化学染色示实验组caspase-3、fas、p53阳性表达率均为100%,对照组caspase-3、fas、p53阳性表达率为13.3%,16.7%,10%,两组比较差异均有统计学意义(P<0.001)。结果表明,腰椎肥厚黄韧带组织中细胞凋亡增加,肥厚黄韧带中细胞凋亡与caspase-3、fas、p53的表达上调具有一定的相关性。 展开更多
关键词 腰椎 黄韧带 黄韧带肥厚 细胞凋亡 CASPASE-3 FAS P53
在线阅读 下载PDF
Claudin-15 overexpression inhibits proliferation and promotes apoptosis of Schwann cells in vitro 预览
12
作者 Jian-Nan Li Zhan Zhang +2 位作者 Guang-Zhi Wu Deng-Bing Yao Shu-Sen Cui 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第1期169-177,共9页
Our previous experiments have discovered that Claudin-15 was up-regulated in Schwann cells of the distal nerve stumps of rat models of sciatic nerve injury.However,how Claudin-15 affects Schwann cell function is still... Our previous experiments have discovered that Claudin-15 was up-regulated in Schwann cells of the distal nerve stumps of rat models of sciatic nerve injury.However,how Claudin-15 affects Schwann cell function is still unknown.This study aimed to identify the effects of Claudin-15 on proliferation and apoptosis of Schwann cells cultured in vitro and explore the underlying mechanisms.Primary Schwann cells were obtained from rats.Claudin-15 in Schwann cells was knocked down using siRNA(siRNA-1 group)compared with the negative control siRNA transfection group(negative control group).Claudin-15 in Schwann cells was overexpressed using pGV230-Claudin-15 plasmid(pGV230-Claudin-15 group).The pGV230 transfection group(pGV230 group)acted as the control of the pGV230-Claudin-15 group.Cell proliferation was analyzed with EdU assay.Cell apoptosis was analyzed with flow cytometric analysis.Cell migration was analyzed with Transwell inserts.The mRNA and protein expressions were analyzed with quantitative polymerase chain reaction assay and western blot assay.The results showed that compared with the negative control group,cell proliferation rate was up-regulated;p-AKT/AKT ratio,apoptotic rate,p-c-Jun/c-Jun ratio,mRNA expression of protein kinase C alpha,Bcl-2 and Bax were down-regulated;and mRNA expression of neurotrophins basic fibroblast growth factor and neurotrophin-3 were increased in the siRNA-1 group.No significant difference was found in cell migration between the negative control and siRNA-1 groups.Compared with the pGV230 group,the cell proliferation rate was down-regulated;apoptotic rate,p-c-Jun/c-Jun ratio and c-Fos protein expression increased;mRNA expression of protein kinase C alpha and Bax decreased;and mRNA expressions of neurotrophins basic fibroblast growth factor and neurotrophin-3 were up-regulated in the pGV230-Claudin-15 group.The above results demonstrated that overexpression of Claudin-15 inhibited Schwann cell proliferation and promoted Schwann cell apoptosis in vitro.Silencing of Claudin-15 had the re 展开更多
关键词 apoptosis Bax cell PROLIFERATION c-Jun Claudin-15 NERVE regeneration peripheral NERVE injury protein kinase C alpha Schwann cells Wallerian DEGENERATION
在线阅读 下载PDF
Protective effects of organic extracts of Alpinia oxyphylla against hydrogen peroxide-induced cytotoxicity in PC12 cells 预览
13
作者 Li-Hong Duan Meng Li +10 位作者 Chun-Bao Wang Qing-Mei Wang Quan-Quan Liu Wan-Feng Shang Ya-Jin Shen Zhuo-Hua Lin Tong-Yang Sun Zheng-Zhi Wu Ying-Hong Li Yu-Long Wang Xun Luo 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第4期682-689,共8页
Alpinia oxyphylla,a traditional herb,is widely used for its neuroprotective,antioxidant and memory-improving effects.However,the neuroprotective mechanisms of action of its active ingredients are unclear.In this study... Alpinia oxyphylla,a traditional herb,is widely used for its neuroprotective,antioxidant and memory-improving effects.However,the neuroprotective mechanisms of action of its active ingredients are unclear.In this study,we investigated the neuroprotective effects of various organic extracts of Alpinia oxyphylla on PC12 cells exposed to hydrogen peroxide-induced oxidative injury in vitro.Alpinia oxyphylla was extracted three times with 95%ethanol(representing extracts 1–3).The third 95%ethanol extract was dried and resuspended in water,and then extracted successively with petroleum ether,ethyl acetate and n-butanol(representing extracts 4–6).The cell counting kit-8 assay and microscopy were used to evaluate cell viability and observe the morphology of PC12 cells.The protective effect of the three ethanol extracts(at tested concentrations of 50,100 and 200μg/mL)against cytotoxicity to PC12 cells increased in a concentration-dependent manner.The ethyl acetate,petroleum ether and n-butanol extracts(each tested at 100,150 and 200μg/mL)had neuroprotective effects as well.The optimum effective concentration ranged from 50–200μg/mL,and the protective effect of the ethyl acetate extract was comparatively robust.These results demonstrate that organic extracts of Alpinia oxyphylla protect PC12 cells against apoptosis induced by hydrogen peroxide.Our findings should help identify the bioactive neuroprotective components in Alpinia oxyphylla. 展开更多
关键词 active INGREDIENTS ALPINIA oxyphylla apoptosis ethanol crude extract fraction hydrogen PEROXIDE nerve regeneration NEUROPROTECTIVE agent NEUROPROTECTIVE effects PC12 cells traditional HERB
在线阅读 下载PDF
双硫仑联合铜离子对人骨肉瘤细胞增殖与凋亡的影响 预览
14
作者 徐朝健 张龙 +2 位作者 程才统 孙晓娟 吕智 《中国组织工程研究》 CAS 北大核心 2020年第1期124-129,共6页
背景:研究表明双硫仑本身具有抗肿瘤活性,可联合铜(Cu)离子在体内外水平对多种肿瘤发挥抑癌作用,但关于双硫仑对骨肉瘤细胞增殖和凋亡作用的影响尚未阐明。目的:探讨双硫仑-Cu在体内外水平对骨肉瘤增殖与凋亡能力的影响以及可能的作用... 背景:研究表明双硫仑本身具有抗肿瘤活性,可联合铜(Cu)离子在体内外水平对多种肿瘤发挥抑癌作用,但关于双硫仑对骨肉瘤细胞增殖和凋亡作用的影响尚未阐明。目的:探讨双硫仑-Cu在体内外水平对骨肉瘤增殖与凋亡能力的影响以及可能的作用机制。方法:实验方案经山西医科大学动物实验伦理委员会批准(批准号为2017LL077)。①体外实验:配置双硫仑在进入人体后的转换物二乙基二硫代氨基甲酸钠(diethyldithiocarbamate,DDTC)和Cu离子的复合物DDTC-Cu(0.5,1,2,3和5μmol/L),设置DDTC单药(5μmol/L)、Cu单药(5μmol/L)和空白对照组。药物处理人骨肉瘤细胞Saos-2细胞和MG-63细胞,CCK8法检测不同浓度DDTC-Cu对Saos-2细胞和MG-63细胞的增殖抑制作用;采用AnnexinV-FITC/PI双染法检测DDTC-Cu对Saos-2细胞凋亡水平变化;②体内实验:取4周龄BALB/c-nu/nu雌性裸鼠共10只,随机分为DDTC-Cu组和对照组。采用异位移植方法,在裸鼠右侧背部皮下注射Saos-2细胞和Matrigel混悬液(1∶1混合),注射量400μL/只;接种2周后,对照组裸鼠腹腔注射地塞米松(0.5mg/kg,隔日1次),DDTC-Cu组裸鼠腹腔注射地塞米松(0.5mg/kg,隔日1次)和DDTC-Cu复合物(10nmol/g,隔日1次);观察两组荷瘤小鼠移植瘤生长情况,绘制瘤体生长曲线。接种5周后麻醉下处死动物,完整取出瘤体,免疫组织化学检测瘤体石蜡切片组织中ki67蛋白的表达水平,Westernblot检测瘤体组织中细胞增殖和凋亡蛋白的表达及JNK通路蛋白表达的变化。结果与结论:①体外实验结果:DDTC-Cu组对骨肉瘤细胞的增殖抑制作用明显高于其他3组;CCK-8实验结果显示DDTC-Cu对骨肉瘤细胞增殖抑制呈剂量依赖性,两株细胞的24h药物半抑制浓度分别为0.337μmol/L和0.487μmol/L;流式细胞学检测结果显示DDTC-Cu可呈剂量依赖性促进Saos-2细胞的凋亡;②体内实验结果:DDTC-Cu组裸鼠移植瘤的体积和质量均小于对照组;免疫组织化学 展开更多
关键词 双硫仑 骨肉瘤 增殖 凋亡 JNK通路
在线阅读 下载PDF
大鼠缺氧复氧损伤神经元钙敏感受体表达水平及其与神经元凋亡的相关性分析 预览
15
作者 张立芳 李博 常快乐 《临床和实验医学杂志》 2019年第14期1479-1483,共5页
目的 分析缺氧复氧损伤神经元钙敏感受体表达水平及其与神经元凋亡的相关性。方法 取新生SD大鼠(出生1 d)脊髓神经元,随机分为A组(正常对照,未进行任何处理)、B组(建立缺氧复氧损伤模型)、C组(缺氧复氧损伤+激动剂GdCl 3)、D组(缺氧复... 目的 分析缺氧复氧损伤神经元钙敏感受体表达水平及其与神经元凋亡的相关性。方法 取新生SD大鼠(出生1 d)脊髓神经元,随机分为A组(正常对照,未进行任何处理)、B组(建立缺氧复氧损伤模型)、C组(缺氧复氧损伤+激动剂GdCl 3)、D组(缺氧复氧损伤+抑制剂NPS-2390)。通过免疫荧光技术对各组大鼠脊髓神经元中钙敏感受体的表达定位进行检测,并用Western blotting法对各组钙敏感受体及凋亡相关蛋白B淋巴细胞瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)表达水平进行检测,通过激光共聚焦显微镜对细胞内游离钙的变化进行检测,同时用TUNEL法对各组细胞凋亡情况进行检测。结果 B组钙敏感受体和细胞内游离钙的表达水平较A组显著升高( P <0.01),C组钙敏感受体和细胞内游离钙表达水平较B组显著升高( P <0.01),D组钙敏感受体和细胞内游离钙表达水平较B组显著下降( P <0.01)。B组细胞凋亡比率较A组显著升高,C组细胞凋亡比率较B组显著升高,D组细胞凋亡比率较B组显著下降( P <0.05)。B组凋亡相关蛋白Bcl-2的表达水平较A组显著下降,Bax和Caspase-3的表达水平较A组显著升高( P <0.05);C组Bcl-2的表达水平较B组显著下降,Bax和Caspase-3的表达水平较B组显著升高( P <0.05);D组Bcl-2的表达水平较B组显著升高,Bax和Caspase-3的表达水平较B组显著下降( P <0.05)。结论 在大鼠缺氧复氧损伤模型中,钙敏感受体在脊髓神经元中的表达水平升高,细胞内游离钙增多,脊髓神经元细胞凋亡比率升高,凋亡相关蛋白的表达水平升高。 展开更多
关键词 大鼠 缺氧复氧损伤 脊髓神经元 钙敏感受体 细胞凋亡 凋亡相关蛋白
在线阅读 下载PDF
Construction of 3β-HSD gene silencing cell line and its effects on apoptosis induced by DEHP
16
作者 王利 《中国医学文摘:内科学分册(英文版)》 2019年第2期74-75,共2页
Objective To construct 3β-HSD gene shRNA lentivirus interference vecto,then transfect into human MCF-7 cells,and construct cell line with 3β-HSD gene silencing,finally to study the effects of 3β-HSD on apoptosis in... Objective To construct 3β-HSD gene shRNA lentivirus interference vecto,then transfect into human MCF-7 cells,and construct cell line with 3β-HSD gene silencing,finally to study the effects of 3β-HSD on apoptosis induced by di-(2-ethylhexyl) phthalate (DEHP).Methods According to the mRNA sequence of 3β-HSD gene provided by GenBank,three interference sequenceswere designed and connected to PLVX-shRNA2-puro afterannealing. 展开更多
关键词 HSD gene silencing cell line APOPTOSIS INDUCED by DEHP CONSTRUCTION of 3 APOPTOSIS
Resveratrol Attenuates Benzo(a)pyrene-Induced Dysfunctions, Oxidative Stress and Apoptosis in Pancreatic Beta-Cells 预览
17
作者 Sefa ?elik Bari? Baysal Serkan ?en 《生命科学与技术进展(英文)》 2019年第11期389-404,共16页
Background: Diabetes mellitus is one of the major health problems for people all over the world today. According to international diabetes federation reports, diabetes affects 382 million people worldwide. Environment... Background: Diabetes mellitus is one of the major health problems for people all over the world today. According to international diabetes federation reports, diabetes affects 382 million people worldwide. Environmental pollutants have deleterious effects on glucose metabolism and cause insulin resistance. We aimed to investigate the effects of the environmental pollutants benzo(a)pyrene, and the therapeutic potential of resveratrol. Methods: 20 μM of benzo(a)pyrene was administered after 48 h of resveratrol (80 μM) application for 24 h in INS-1 (832/13) insulinoma cells. The cells were treated with 20 μM benzo(a)pyrene for 24 hours after 48 hours initial preconditions with 10 μM resveratrol. Oxidative stress status, insulin secretion and apoptosis were analyzed by molecular techniques. Results: Though resveratrol increased the antioxidant status which was decreased by benzo(a)pyrene, interestingly, it increased the oxidative status. Resveratrol increased benzo(a)pyrene-depleted reduced glutathione levels to the control level. The mRNA expression levels of beta-cell functions associated with genes insulin-1, insulin-2 and sirtuin-1 were upregulated by resveratrol. Resveratrol treatment elevated the insulin concentration of culture medium, and the mRNA expression of forkhead box protein-1 gene. Resveratrol upregulated benzo(a)pyrene-downregulated p53 gene expression. On the other hand, benzo(a)pyrene-downregulated mRNA expression of B-cell lymphoma-2 was induced by resveratrol treatment. Conclusion: The data showed that resveratrol could reverse the oxidative alterations, functional impairments and the carcinogenetic effects of benzo(a)pyrene in pancreas beta-cells. 展开更多
关键词 Benzo(a)pyrene INS-1 (832/13) INSULINOMA Cell INSULIN APOPTOSIS Oxidative Stress RESVERATROL
在线阅读 免费下载
Livin及Caspase-3在下咽癌组织中的表达及临床意义 预览
18
作者 丁凌雁 唐朝晖 +1 位作者 李立志 黄洪林 《华夏医学》 CAS 2019年第3期72-76,共5页
目的:探讨Livin及Caspase-3在下咽癌组织中的表达及临床意义。方法:选择经病理学确诊60例下咽癌患者的石蜡癌组织标本及癌旁组织标本,同时收集同期下咽良性疾病患者石蜡组织标本20例。采用免疫组织化学法对下咽癌组织、癌旁组织及同期... 目的:探讨Livin及Caspase-3在下咽癌组织中的表达及临床意义。方法:选择经病理学确诊60例下咽癌患者的石蜡癌组织标本及癌旁组织标本,同时收集同期下咽良性疾病患者石蜡组织标本20例。采用免疫组织化学法对下咽癌组织、癌旁组织及同期下咽良性疾病患者石蜡组织中Livin及Caspase-3蛋白进行检测,探讨Livin及Caspase-3表达情况与临床病理特征的关系。结果:下咽癌组织中Livin蛋白的阳性表达率(81.67%)高于癌旁组织(35.0%)和下咽良性疾病组织(0),P均<0.05。Caspase-3蛋白的阳性表达率(36.67%)低于癌旁组织(46.67%)和下咽良性疾病组织(90.0%),P均<0.05。下咽癌组织中Livin蛋白表达与淋巴结转移有关(P<0.05),而与TNM分期、分化程度无关(P均> 0.05)。下咽癌组织中Caspase-3蛋白表达与分化程度、淋巴结转移有关(P均<0.05),而与TNM分期无关(P>0.05)。下咽癌组织中,Livin与Caspase-3蛋白表达呈负相关(r=-0.355,P=0.005)。结论:Livin蛋白可抑制Caspase-3蛋白的活性,从而抑制细胞凋亡和促进细胞增殖,加速细胞的恶性转化和下咽癌的发生。 展开更多
关键词 下咽癌 LIVIN CASPASE-3 凋亡 凋亡抑制因子
在线阅读 下载PDF
异柠檬酸脱氢酶1对替莫唑胺干预下U87细胞细胞凋亡的影响 预览
19
作者 王举波 权瑜 +1 位作者 吕健 董丹凤 《贵州医科大学学报》 CAS 2019年第8期892-897,共6页
目的:探讨人异柠檬酸脱氢酶1(mIDH1)基因突变对替莫唑胺(TMZ)干预下脑胶质瘤U87细胞凋亡的影响。方法:用基因重组技术构建真核表达载体mIDH1/wIDH1,转染技术构建目的基因的U87细胞的稳转细胞系,采用流式细胞术检测TMZ干预24h后的细胞凋... 目的:探讨人异柠檬酸脱氢酶1(mIDH1)基因突变对替莫唑胺(TMZ)干预下脑胶质瘤U87细胞凋亡的影响。方法:用基因重组技术构建真核表达载体mIDH1/wIDH1,转染技术构建目的基因的U87细胞的稳转细胞系,采用流式细胞术检测TMZ干预24h后的细胞凋亡率;构建裸鼠移植瘤模型,采用免疫组织化学法(Westernblot)检测mIDH1对TMZ干预U87细胞24h时及TMZ连续灌胃5d时裸鼠移植瘤相关凋亡蛋白Caspase-3、Caspase-9、Bax及Bcl-2的表达水平。结果:成功构建胶质瘤稳转细胞系,流式细胞术结果显示,mIDH1能提高TMZ作用后U87细胞的凋亡率,也能上调TMZ干预24h时U87细胞及TMZ连续灌胃5d时裸鼠移植瘤中Caspase-3、Caspase-9、Bax蛋白表达水平,下调Bcl-2蛋白表达水平(P<0.05)。结论:mIDH1通过上调TMZ作用的U87细胞、裸鼠移植瘤组织的Caspase-3、Caspase-9、Bax表达、下调Bcl-2表达促进胶质瘤细胞凋亡。 展开更多
关键词 胶质瘤细胞 异柠檬酸脱氢酶1 凋亡 细胞 凋亡相关蛋白 替莫唑胺
在线阅读 下载PDF
miR-92a对宫颈癌细胞增殖凋亡影响及其机制 预览
20
作者 王利娟 谷丽娟 孙颖川 《青岛大学学报(医学版)》 CAS 2019年第4期406-410,共5页
目的探讨miR-92a对宫颈癌细胞增殖凋亡的影响及其机制。方法应用逆转录-聚合酶链反应(RT-PCR)检测宫颈癌细胞系中miR-92a的表达情况。将细胞分为空白对照组(未转染)、miR-92a抑制物阴性对照组(转染miR-92a inhibitor NC)和miR-92a抑制物... 目的探讨miR-92a对宫颈癌细胞增殖凋亡的影响及其机制。方法应用逆转录-聚合酶链反应(RT-PCR)检测宫颈癌细胞系中miR-92a的表达情况。将细胞分为空白对照组(未转染)、miR-92a抑制物阴性对照组(转染miR-92a inhibitor NC)和miR-92a抑制物组(转染miR-92a inhibitor),并以RT-PCR检测转染效果,采用MTT法检测细胞增殖,流式细胞仪检测细胞凋亡,Western blot检测细胞中基质金属蛋白酶2(MMP-2)和生存素(Survivin)蛋白的表达。结果与正常上皮293T细胞相比,miR-92a在宫颈癌Hela、C33A和Caski细胞中的表达水平均明显升高(t=6.446~14.544,P<0.001),其中以Hela细胞上升最为显著。与空白对照组比较,转染miR-92a inhibitor使Hela细胞中miR-92a的表达、A值、MMP-2和Survivin蛋白表达均显著下降,细胞凋亡率显著升高(t=3.479~22.18,P<0.05);而转染miR-92a inhibitor NC后差异无显著性(P>0.05)。结论 miR-92a在宫颈癌细胞中高表达,干扰其表达可以抑制细胞生长,其作用机制可能与下调MMP-2和Survivin蛋白表达有关。 展开更多
关键词 宫颈肿瘤 微RNAS 细胞增殖 细胞凋亡 基质金属蛋白酶2 凋亡调节蛋白质类
在线阅读 下载PDF
上一页 1 2 250 下一页 到第
使用帮助 返回顶部 意见反馈