【摘 要】
:
Objective: Cerebrovascular disease (CVD) is a cerebral dysfunction caused by a variety of vascular encephalopathy,diabetes-induced cerebrovascular disease is a new concept proposed in recent years,def
【机 构】
:
Department of Geriatrics, Affiliated Hospital of Nantong University, Nantong, Jiangsu,226001, China
【出 处】
:
中国脑卒中大会2016暨第六届全国心脑血管病论坛、2016中国脑卒中大会中西医结合心脑血管病论坛、世界中医药学会联合会脑
论文部分内容阅读
Objective: Cerebrovascular disease (CVD) is a cerebral dysfunction caused by a variety of vascular encephalopathy,diabetes-induced cerebrovascular disease is a new concept proposed in recent years,defined as the intracranial macrovascular and microvascular disease based on a series of metabolic disorders of sugar,fat,protein,etc,clinically presented with ischemic cerebrovascular disease,cerebral hemorrhage or cerebral atrophy.However,researches on diabetic cerebral microangiopathy are few.The pathophysiology of diabetic microangiopathy in cerebral ischemic cerebrovascular disease is still not clear.Statins are 3-hydroxy-3-methyl glutaryl coenzyme A (HMG-CoA) reductase inhibitors that are widely used to treat hypercholesterolemia and other cardiovascular diseases.Beyond this well-defined mode of action for statins,several clinical trials have demonstrated that this class of drugs can protect against CVD through an additional mechanism that is independent of cholesterol lowering.Our study used cerebral microvascular endothelial cells (MVECs) cultured in vitro as the cell model,then incubate them with high glucose,and observed HMGB-1 released by endothelium to find its relationship with high glucose-induced cerebral microvascular endothelial damage.Besides,we co-incubated MVECs with simvastatin & high glucose to investigate the protective effect of simvastatin on endothelial cells,to observe the effects of high glucose and simvastatin on the growth of cerebral microvascular endothelial cells (MVECs) and the releasing of high mobility group box 1 (HMGB-1),and to investigate the mechanism of high glucose-induced damage as well as the protective effect of simvastatin on MVECs.
其他文献
目的:探讨中国青岛地区脑梗死患者GC(维生素D结合蛋白)和VDR(维生素D受体)基因多态性,并进一步探讨遗传因素对动脉粥样硬化颅内外选择性损害的影响。方法:选取272例LAA(大动脉粥样硬化性卒中)型脑梗死患者、87例SAO(小动脉闭塞性脑梗死)患者及175例同期非脑梗死人群,从VDR和GC基因中分别选取2个代表性单核酸多态性VDR[SNPs,rs2228570、rs1544410]和GC[SNP
目的:对载脂蛋白E基因敲出小鼠(ApoE-/-小鼠)颈动脉粥样硬化斑块中Toll样受体4(TLR4)、NF-κB、肿瘤坏死因子(TNF-α)和白介素(IL-1β)的表达水平进行研究分析,以探讨该炎症通路在动脉粥样硬化发病过程中所发生的变化及其意义。方法:ApoE-/-小鼠随机分为对照组(12只)和模型组(12只)。对照组给予正常饮食,做假手术。模型组给予高脂饮食并做右颈总动脉外置硅胶管术。两组小鼠
目的:探讨血浆α2巨球蛋白(α2-MG)水平与小动脉闭塞性脑梗死(SAO)的发生及脑部白质损害(WMLs)程度的关系。方法:选取符合TOAST分型的SAO患者58例,大动脉粥样硬化性脑梗死(LAA)患者56例,健康对照组53例,应用酶联免疫吸附测定法(ELISA)检测上述研究对象的血浆α2-MG浓度。应用F检验比较三组间血浆α2-MG水平的差异,应用多元Logistic回归判断SAO的独立危险因素
目的:探讨血浆miRNA作为脑动脉粥样硬化血浆标志物的可行性。方法:选取41例无症状脑动脉粥样硬化患者(AS组)、57例大动脉粥样硬化性(Large artery atherosclerotic,LAA)脑梗死患者(LAA组)和50例同期健康查体者(control组),实时荧光定量PCR(quantitative real-time PCR,qRT-PCR)检测受试者血浆中miR-126、miR-
Background: Circular RNAs (circRNAs) are an enigmatic class of endogenous RNAs,and play a role in regulation of gene expression.Their diagnostic value and pathogenesis of Leukoaraiosis (LA) was undisc
目的:研究基质金属蛋白酶-2、9(MMP-2、9)与动脉粥样硬化性脑梗死初发及复发的相关性.方法:选取初发脑梗死350例,复发脑梗死340例,正常健康组360例.ELISA法检测MMP-2、9的含量,比较三组间MMP-2、9含量的差异.
目的:建立小鼠慢性脑缺血模型并探讨DHA对小鼠慢性脑缺血损伤的可能保护作用。材料与方法:采用右侧颈总动脉永久结扎建立小鼠慢性脑缺血模型(rUCCAO)。将小鼠分为对照组(sham组)、rUCCAO模型组、DHA给药组(造模后24h开始每日注射DHA 35mg/kg一次,共20天)。观察慢性脑缺血后60d各组动物的神经缺损症状并评分。动物行为学变化采用新事物识别和水迷宫实验检测,评价动物学习记忆损害
目的:miR-27a是15~22 nt的非编码RNA,在转录后水平调节靶基因的表达,但其在脑缺血再灌注损伤损伤中的作用仍不清。方法:在小鼠脑缺血再灌注损伤模型中,缺血1h时将miR-27a类似物或拮抗物注入左侧脑室,再灌注24 h后,分别检测miR-27a的表达水平,并通过梗死面积、神经功能评分和炎症因子IL-1β,TNF-α和NO的释放来评估其神经损伤作用。采用Targetscan预测miR-2
目的:研究基质金属蛋白酶9 (MMP-9)基因启动子区R279Q和R668Q多态性与动脉粥样硬化性脑梗死初发及复发的相关性。方法:选取初发脑梗死350例,复发脑梗死340例,正常健康组360例。采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)分析法对MMP-9基因R279Q和R668Q多态性进行分析;ELISA法检测MMP-9的含量,比较三组间MMP-9基因多态性频率分布及含量的差异。
目的:探讨大脑中动脉粥样硬化斑块内出血及超敏血清C反应蛋白(hs-CRP)、同型半胱氨酸(Hcy)、尿酸(UA)水平与急性脑梗死相关性.方法:回顾性分析3D-TOF MRA显示大脑中动脉主干M1段高度狭窄(狭窄>=70%) 136例患者临床资料及高分辨率MRI表现.分析大脑中动脉斑块内出血、hs-CRP、Hcy及UA水平与急性脑梗死相关性.计数资料采用x2检验,计量资料采用t检验,P<0.05为差