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Hyperoside protects the blood-brain barrier from neurotoxicity of amyloid beta 1–42 被引量:5
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作者 Chen-Yang Liu Kuan Bai +2 位作者 Xiao-Hui Liu Li-Mi Zhang Gu-Ran Yu 《Neural Regeneration Research》 SCIE CAS CSCD 2018年第11期1974-1980,共7页
Mounting evidence indicates that amyloid β protein(Aβ) exerts neurotoxicity by disrupting the blood-brain barrier(BBB) in Alzheimer's disease. Hyperoside has neuroprotective effects both in vitro and in vivo ag... Mounting evidence indicates that amyloid β protein(Aβ) exerts neurotoxicity by disrupting the blood-brain barrier(BBB) in Alzheimer's disease. Hyperoside has neuroprotective effects both in vitro and in vivo against Aβ. Our previous study found that hyperoside suppressed Aβ1-42-induced leakage of the BBB, however, the mechanism remains unclear. In this study, bEnd.3 cells were pretreated with 50, 200, or 500 μM hyperoside for 2 hours, and then exposed to Aβ1-42 for 24 hours. Cell viability was determined using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay. Flow cytometry and terminal deoxynucleotidyl transferase-mediated d UTP nick-end labeling assay were used to analyze cell apoptosis. Western blot assay was carried out to analyze expression levels of Bax, Bcl-2, cytochrome c, caspase-3, caspse-8, caspase-9, caspase-12, occludin, claudin-5, zonula occludens-1, matrix metalloproteinase-2(MMP-2), and MMP-9. Exposure to Aβ1-42 alone remarkably induced bEnd.3 cell apoptosis; increased ratios of cleaved caspase-9/caspase-9, Bax/Bcl-2, cleav ed caspase-8/caspase-8, and cleaved caspase-12/caspase-12; increased expression of cytochrome c and activity of caspase-3; diminished levels of zonula occludens-1, claudin-5, and occludin; and increased levels of MMP-2 and MMP-9. However, hyperoside pretreatment reversed these changes in a dose-dependent manner. Our findings confirm that hyperoside alleviates fibrillar Aβ1-42-induced BBB disruption, thus offering a feasible therapeutic application in Alzheimer's disease. 展开更多
关键词 nerve regeneration Alzheimer's disease amyloid beta 1-42 blood-brain barrier bEnd.3 cells tight junction proteins HYPEROSIDE ANTI-APOPTOSIS neural regeneration
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Crocetin Prevents Amyloid <i>β</i><sub>1-42</sub>-Induced Cell Death in Murine Hippocampal Cells 被引量:1
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作者 Yuta Yoshino Mitsue Ishisaka +3 位作者 Naofumi Umigai Masamitsu Shimazawa Kazuhiro Tsuruma Hideaki Hara 《Pharmacology & Pharmacy》 2014年第1期37-42,共6页
Crocetin is an aglycon of carotenoid extracted by saffron stigmas (Crocus sativus L.) and known to have a potent anti-oxidative effect. Amyliod β (Aβ), hallmark of Alzheimer’s disease, is reported to have neurotoxi... Crocetin is an aglycon of carotenoid extracted by saffron stigmas (Crocus sativus L.) and known to have a potent anti-oxidative effect. Amyliod β (Aβ), hallmark of Alzheimer’s disease, is reported to have neurotoxicity partly via oxidative stress. In this study, we investigated the effect of crocetin on hippocampal HT22 cell death induced by Aβ1-42. Furthermore, to clarify the mechanism underlying the protective effects of crocetin against Aβ1-42- induced cell death, we measured reactive oxygen species (ROS) production by CM-H2DCFDA kit assay. Crocetin at 1 -10 μM protected HT22 cells against Aβ1-42-induced neuronal cell death and decreased ROS production increased by Aβ1-42. These results that crocetin has the potent neuroprotective effect against Aβ1-42-induced cytotoxicity in hippocampal cells by attenuating oxidative stress, suggest that crocetin may provide a useful therapeutic strategy against Aβ-related disorders. 展开更多
关键词 Alzheimer’s Disease amyloid β1-42 CROCETIN HT22 Oxidative Stress
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前列地尔联合吡拉西坦对老年认知障碍患者可溶性细胞间黏附分子-1和β-淀粉样蛋白1-42的影响 被引量:3
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作者 崔璐莎 董晓柳 +3 位作者 王增英 赵蕊 刘海艳 佟久芬 《西北药学杂志》 CAS 2021年第1期122-126,共5页
目的探究前列地尔联合吡拉西坦对老年认知功能障碍患者血清可溶性细胞间黏附分子-1(sICAM-1)及β-淀粉样蛋白1-42(Aβ1-42)表达的影响。方法选取114例老年认知功能障碍患者,采用随机数表法分为观察组和对照组。对照组患者口服吡拉西坦片... 目的探究前列地尔联合吡拉西坦对老年认知功能障碍患者血清可溶性细胞间黏附分子-1(sICAM-1)及β-淀粉样蛋白1-42(Aβ1-42)表达的影响。方法选取114例老年认知功能障碍患者,采用随机数表法分为观察组和对照组。对照组患者口服吡拉西坦片,每日3次,每次4片;观察组患者在对照组治疗的基础上静脉滴注前列地尔10μg,每日1次,共治疗1个月。对比2组患者治疗后的疗效、治疗前后的认知功能、日常生活能力变化情况、事件相关电位(ERPP300)、脑电图(EEG)、血清sICAM-1及Aβ1-42的变化情况。结果观察组患者治疗有效率较对照组显著上升(P<0.05);治疗前2组患者的认知功能及日常生活评分无明显差异,治疗后观察组患者的认知功能评分、日常生活能力评分较对照组均明显改善(P<0.05);治疗前2组患者的ERPP300及EEG无明显差异,治疗后观察组患者的ERPP300潜伏期较对照组明显下降,波幅较对照组明显上升,且EEG异常率较对照组明显下降(P<0.05);治疗前2组患者血清sICAM-1及Aβ1-42表达无明显差异,治疗后2组患者血清sICAM-1及Aβ1-42表达均明显下降,且观察组较对照组明显下降(P<0.05)。结论前列地尔联合吡拉西坦治疗老年认知功能障碍较单用吡拉西坦治疗疗效更好,能改善患者的EEG、ERPP300、血清sICAM-1及Aβ1-42表达。 展开更多
关键词 前列地尔 吡拉西坦 老年认知功能障碍 可溶性细胞间黏附分子-1 β-淀粉样蛋白1-42
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Effect of Panax notoginseng saponins on the expression of beta-amyloid protein in the cortex of the parietal lobe and hippocampus, and spatial learning and memory in a mouse model of senile dementia 被引量:9
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作者 Zhenguo Zhong Dengpan Wu Liang Lu Jinsheng Wang Wenyan Zhang Zeqiang Qu 《Neural Regeneration Research》 SCIE CAS CSCD 2008年第12期1297-1303,共7页
BACKGROUND: The pharmacological actions of Panax notoginseng saponins (PNS) lie in removing free radicals, anti-inflammation and anti-oxygenation. It can also improve memory and behavior in rat models of Alzheime... BACKGROUND: The pharmacological actions of Panax notoginseng saponins (PNS) lie in removing free radicals, anti-inflammation and anti-oxygenation. It can also improve memory and behavior in rat models of Alzheimer's disease. OBJECTIVE: Using the Morris water maze, immunohistochemistry, real-time PCR and RT-PCR, this study aimed to measure improvement in spatial learning, memory, expression of amyloid precursor protein (App) and β -amyloid (A β ), to investigate the mechanism of action of PNS in the treatment of AD in the senescence accelerated mouse-prone 8 (SAMP8) and compare the effects with huperzine A. DESIGN, TIME AND SETTING: A completely randomized grouping design, controlled animal experiment was performed in the Center for Research & Development of New Drugs, Guangxi Traditional Chinese Medical University from July 2005 to April 2007. MATERIALS: Sixty male SAMP8 mice, aged 3 months, purchased from Tianjin Chinese Traditional Medical University of China, were divided into four groups: PNS high-dosage group, PNS low-dosage group, huperzine A group and control group. PNS was provided by Weihe Pharmaceutical Co., Ltd. (batch No.: Z53021485, Yuxi, Yunan Province, China). Huperzine A was provided by Zhenyuan Pharmaceutical Co., Ltd. (batch No.: 20040801, Zhejiang, China). METHODS: The high-dosage group and low-dosage group were treated with 93.50 and 23.38 mg/kg PNS respectively per day and the huperzine A group was treated with 0.038 6 mg/kg huperzine A per day, all by intragastric administration, for 8 consecutive weeks. The same volume of double distilled water was given to the control group. MAIN OUTCOME MEASURES: After drug administration, learning and memory abilities were assessed by place navigation and spatial probe tests. The recording indices consisted of escape latency (time-to-platform), and the percentage of swimming time spent in each quadrant. The number of A β 1-40, A β 1-42 and App immunopositive neurons in the brains of SAMP8 mice was analyzed by immunohistochemistry. The mRNA content ofApp, tau, acetylcholinesterase, and synaptophysin (Syp) was tested by real time PCR and RT-PCR. RESULTS: The PCR results show that PNS can downregulate the expression of the App gene and upregulate the expression of the Syp gene in the parietal cortex and hippocampus of SAMP8 mice. The therapeutic effects of the PNS high-dosage group were greater than those of the PNS low-dosage group and the huperzine A group (P 〈 0.05). The results of the Morris water maze and immunohistochemistry indicated that PNS can improve the capacity for spatial learning and memory in SAMP8 mice, and reduce the content of A β 1-40, A β 1-42 and expression of App in the brains of SAMP8 mice. The therapeutic effects of the PNS high-dosage group were greater than that of the PNS low-dosage group and the huperzine A group (P 〈 0.05). CONCLUSION: These results support the hypothesis that PNS plays a therapeutic and protective role on the pathological lesions and learning dysfunction of Alzheimer's disease. The therapeutic effects of PNS for Alzheimer's disease are possibly achieved through downregulating the expression of the App gene and upregulating the expression of the Syp gene. The therapeutic effects of PNS are dose-dependent and are greater than the effect of huperzine A. 展开更多
关键词 Alzheimer's disease Panax notoginseng saponins learning and memory β -amyloid precursor protein 1-40 β -amyloid precursor protein 1-42 amyloid β -peptide SYNAPTOPHYSIN senescence accelerated mouse-prone 8
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Copper(Ⅱ) ions-immobilized virus-like hollow covalent organic frameworks for highly efficient capture and sensitive analysis of amyloid beta-peptide 1–42 by MALDI-MS
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作者 Wende Ma Chao Zhong +6 位作者 Juan Lin Zhuling Chen Guorong Li Wei Tong Yijing Wu Lan Zhang Zian Lin 《Chinese Chemical Letters》 SCIE CAS CSCD 2022年第12期5174-5179,共6页
Amyloid beta-peptide 1-42(Aβ1-42)is one of the biomarkers of Alzheimer's disease,and its selective capture and quantitative detection are important for diagnosis and treatment of Alzheimer's disease.Herein,co... Amyloid beta-peptide 1-42(Aβ1-42)is one of the biomarkers of Alzheimer's disease,and its selective capture and quantitative detection are important for diagnosis and treatment of Alzheimer's disease.Herein,copper(Ⅱ)ions-immobilized virus-like hollow covalent organic frameworks(V-HCOFs@Cu^(2+))were synthesized by a facile approach.The as-prepared V-HCOFs@Cu^(2+)showed unique morphology,ultra-high specific surface(2552 m^(2)/g),uniform mesoporous structure(3.2 nm),superior chemical stability and abundant binding sites.Based on these excellent properties,the V-HCOFs@Cu^(2+)could be adopted as an ideal enrichment probe for highly efficient capture of Aβ1-42,exhibiting high adsorption capacity(320 mg/g),and fast adsorption equilibration time(3 min).In addition,an attractive approach of the V-HCOFs@Cu^(2+)-based matrix-assisted laser desorption/ionization mass spectrometry(MALDI-MS)was developed for the rapid screening and quantitative analysis of Aβ1-42 in human serum by using C-peptide as an internal standard,which exhibited low limit of detection(LOD,0.2 fmol/μL),and satisfactory recovery.This work provides an alternative solution for enrichment of biomarkers and also offers the potential applications of COFs in clinical analysis. 展开更多
关键词 Virus-like hollow covalent organic frameworks Metal ion immobilization amyloidβ-peptide 142 CAPTURE Matrix-assisted laser desorption ionization mass spectrometry
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Kallikrein-related peptidases 6 and 10 are elevated in cerebrospinal fluid of patients with Alzheimer’s disease and associated with CSF-TAU and FDG-PET 被引量:3
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作者 Oliver Goldhardt Inanna Warnhoff +7 位作者 Igor Yakushev Ilijana Begcevic Hans Förstl Viktor Magdolen Antoninus Soosaipillai Eleftherios Diamandis Panagiotis Alexopoulos Timo Grimmer 《Translational Neurodegeneration》 SCIE CAS 2019年第1期304-316,共13页
Background:Alterations in the expression of human kallikrein-related peptidases(KLKs)have been described in patients with Alzheimer’s disease(AD).We elucidated the suitability of KLK6,KLK8 and KLK10 to distinguish AD... Background:Alterations in the expression of human kallikrein-related peptidases(KLKs)have been described in patients with Alzheimer’s disease(AD).We elucidated the suitability of KLK6,KLK8 and KLK10 to distinguish AD from NC and explored associations with established AD biomarkers.Methods:KLK levels in cerebrospinal fluid(CSF),as determined by ELISA,were compared between 32 AD patients stratified to A/T/(N)system with evidence for amyloid pathology and of 23 normal controls with normal AD biomarkers.Associations between KLK levels and clinical severity,CSF and positron emission tomography(PET)based AD biomarkers were tested for.Results:Levels of KLK6 and KLK10 were significantly increased in AD.KLK6 differed significantly between AD A+/T+/N+and AD A+/T−/N+or NC with an AUC of 0.922.CSF pTau and tTau levels were significantly associated with KLK6 in AD.Conclusions:KLK6 deserves further investigations as a potential biomarker of Tau pathology in AD. 展开更多
关键词 Alzheimer’s disease(AD) Kallikrein-like peptidase(KLK) KLK6 KLK8 KLK10 Cerebral amyloid load Cerebrospinal fluid(CSF) amyloid 1-42 1-42 42 Tau protein Total tau tTau Phospho tau pTau Positron emission tomography(PET)
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Can blood amyloid levels be used as a biomarker for Alzheimer's disease?
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作者 Yuan-Han Yang Rocksy FV Situmeang Paulus Anam Ong 《Brain Science Advances》 2021年第1期17-25,共9页
Alzheimer’s disease(AD)increasingly affects society due to aging populations.Even at pre-clinical stages,earlier and accurate diagnoses are essential for optimal AD management and improved clinical outcomes.Biomarker... Alzheimer’s disease(AD)increasingly affects society due to aging populations.Even at pre-clinical stages,earlier and accurate diagnoses are essential for optimal AD management and improved clinical outcomes.Biomarkers such as beta-amyloid(Aβ)or tau protein in cerebrospinal fluid(CSF)have been used as reliable markers to distinguish AD from non-AD,and predicting clinical outcomes,to attain these goals.However,given CSF access methods’invasiveness,these biomarkers are not used extensively in clinical settings.Blood Aβhas been proposed as an alternative biomarker since it is less invasive than CSF;however,sampling heterogeneity has limited its clinical applicability.In this review,we investigated blood Aβas a biomarker in AD and explored how Aβcan be facilitated as a viable biomarker for successful AD management. 展开更多
关键词 Alzheimer’s disease amyloid precursor protein 1-40 1-42 apolipoprotein E cerebrospinal fluid plasma
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