【摘 要】
:
Following ischemic stroke, blood-brain barrier (BBB) is disrupted and is further aggravated with the corresponding incidence of hyperlipidemia.BBB breakdown promotes inflammation infiltration into the
【机 构】
:
State Key Laboratory of Natural Medicines, Department of Physiology, China Pharmaceutical University
【出 处】
:
2016第十一届心血管药理专业委员会全国心脑血管药理学术会议
论文部分内容阅读
Following ischemic stroke, blood-brain barrier (BBB) is disrupted and is further aggravated with the corresponding incidence of hyperlipidemia.BBB breakdown promotes inflammation infiltration into the brain, which exacerbates cerebral ischemic injury as a result.
其他文献
目的:活性氧(ROS)在细胞内积聚引起的氧化应激是心脏缺血再灌注(I/R)损伤的重要病理生理过程,转录因子Egr-1被认为是再灌注损伤各通路的共同分子基础.本研究在心肌来源H9c2细胞及心脏微血管内皮细胞缺氧复氧(H/R)模型—心脏I/R体外模型上,探讨ROS/JNK/Egr-1信号通路是否存在及对心肌I/R损伤具有一系列保护作用的新化合物N-正丁基氟哌啶醇(F2)是否对此通路具有调节作用.
Background: Vascular endothelial dysfunction is the closely related determinant of ischemic heart disease (IHD).Endothelial dysfunction and ischemia/reperfusion injury (IRI) have been associated with
We found previously that acute phase protein orosomucoid reacts to fatigue and activates C-C chemokine receptor type 5 to increase muscle glycogen storage and enhance muscle endurance.To explore the u
Introduction: Glycogen synthase kinase-3 (GSK3) is composed of two isoforms, GSK3-α and-β, which reveals a new component to function differently in glucose homeostasis and promoting inflammation in mu
QT prolongation, a potential risk for arrhythmias, may result from the polymorphism of genes relevant to heart cell repolarization.Another noted cause of QT prolongation is administration of chemical
目的:研究DRAM1在心肌缺血损伤中的作用及机制.方法:行大鼠左前降支冠状动脉永久性结扎术建立大鼠急性心肌梗死模型后,在结扎处附近梗死周边区注射过表达DRAM1腺病毒或阴性对照腺病毒.通过免疫印迹和免疫荧光实验检测DRAM1的表达变化.21天后,超声心动图检测大鼠左心室功能;HE染色和Masson染色观察心肌重构情况;Tunel检测心肌细胞凋亡;毛细血管密度测定观察血管新生;透射电镜观察自噬体和自
The Ca2+-activated C1-channel (CaCC) plays a crucial role in various physiological functions.Recent evidences suggest TMEM16A encodes CaCC in various cells, including endothelial cells.However, the ro
目的:观察伊桐苷的抗氧化作用及其对创伤性脑损伤(TBI)的保护机制.方法:60只SD大鼠随机分为正常对照组、模型对照组、伊桐苷40g/kg组、伊桐苷80g/kg组、伊桐苷160g/kg组、依达拉奉0.005g/kg阳性对照组.应用自由落体击打(Feeney法)造成大鼠创伤性脑损伤模型,伊桐苷治疗组造模后继续给药14天,造模14天后取脑.
Rationale: Cerebral arteries undergo vascular remodeling in the setting of hypertension,but the precise mechanisms remain incompletely understood.Objective: This study was conducted to explore the rol
目的:研究calpain在低氧诱导肺动脉高压肺血管重构中的作用及机制.方法:SD大鼠随机分为低氧组和对照组.通过插管法测定大鼠右心室收缩压及肺动脉平均压,通过右心室/(左心室+室间隔)比值评价右心肥厚指数,通过HE染色检测血管重构情况,实时荧光定量PCR及Westem Blot检测肺动脉CAPN-1、CAPN-2和CAPN mRNA及蛋白表达.原代培养的大鼠肺动脉平滑肌细胞,分为4组:对照组、对照