The changes of blood-brain barrier(BBB)permeability following brain injury werestudied quantitatively by using colloidal gold(CG)particles of various sizes as tracers in 57 rab-bits.In addition,water content in brain ...The changes of blood-brain barrier(BBB)permeability following brain injury werestudied quantitatively by using colloidal gold(CG)particles of various sizes as tracers in 57 rab-bits.In addition,water content in brain tissues was determined.The brain-injured rabbits re-ceived intravenous injection of anisodamine in a dose of 0.3 mg/kg BW at 5rain or 3h after braininjury,and the effect of anisodamine on aherations of BBB permeability and water content of thebrain tissue after brain injury was investigated.The results indicated that an increase of BBBpermeability began at 30min after injury with only a few of 5nm CG tracers present in the endo-cytic pits and endothelial microvilli,and there were 10nm CG tracers passing through the BBB at3 h after brain injury.The increase of BBB permeability reached its peak at 6 h after brain in-jury.More 15nm CG tracers penetrated the BBB by way of pinocytotic vesicule transportationand opening of tight junctions between endothelial cells.The water content in the brain tissueincreased,which was closely correlated to the above-mentioned EBB permeability and giving ad-vantages to the treatment of traumatic brain edema in the present study.展开更多
目的探讨长链非编码RNA(lncRNA)-N1LR在脑缺血再灌注损伤后血脑屏障的作用机制。方法原代小鼠脑微血管内皮细胞常规培养,经氧糖剥夺/复糖复氧(OGD/R)处理模拟脑缺血再灌注损伤,实验分对照组、OGD组、lncRNA-N1LR过表达组(OGD处理后转染...目的探讨长链非编码RNA(lncRNA)-N1LR在脑缺血再灌注损伤后血脑屏障的作用机制。方法原代小鼠脑微血管内皮细胞常规培养,经氧糖剥夺/复糖复氧(OGD/R)处理模拟脑缺血再灌注损伤,实验分对照组、OGD组、lncRNA-N1LR过表达组(OGD处理后转染质粒lncRNA-N1LR过表达)、lncRNA-N1LR沉默组(OGD处理后转染质粒lncRNA-N1LR沉默)。采用逆转录聚合酶链反应检测各组中lncRNA-N1LR mRNA、紧密连接蛋白5(claudin-5)及闭合蛋白(occludin)mRNA表达水平;异硫氰酸荧光素-葡聚糖(FITC-dextran)渗透法检测血脑屏障通透性;免疫蛋白印迹法检测claudin-5、occludin蛋白表达。结果与对照组比较,OGD组lncRNA-N1LR mRNA、occludin、claudin-5 mRNA表达水平下降(0.31±0.01 vs 1.00±0.10,0.42±0.03 vs 1.01±0.13,0.38±0.03 vs 1.00±0.15,P<0.05),血脑屏障FITC-dextran通透性明显升高(58.79±3.04 vs 8.87±0.63,P<0.01)。与OGD组比较,lncRNA-N1LR过表达组lncRNA-N1LR mRNA、occludin、claudin-5 mRNA表达水平升高(0.67±0.07 vs 0.31±0.01,0.92±0.02 vs 0.42±0.03,0.70±0.08 vs 0.38±0.03,P<0.05),血脑屏障FITC-dextran通透性降低(41.57±2.43 vs 58.79±3.04,P<0.05)。与OGD组比较,lncRNA-N1LR沉默组lncRNA-N1LR mRNA、occludin、claudin-5 mRNA表达水平降低(0.21±0.02 vs 0.31±0.01,0.31±0.03 vs 0.42±0.03,0.22±0.02 vs 0.38±0.03,P<0.05),血脑屏障FITC-dextran通透性升高(72.34±1.43 vs 58.79±3.04,P<0.05)。结论LncRNA-N1LR上调可能通过降低血脑屏障通透性发挥神经保护作用。展开更多
目的探究阿托伐他汀对高血糖诱导的小鼠脑缺血后出血转化(HT)的作用及机制。方法36只SPF级雄性C57BL/6小鼠随机分为假手术组、HT模型组和阿托伐他汀组,每组12只。比较各组小鼠神经功能评分、死亡率、HT发生率、HT分级评分,苏木精-伊红...目的探究阿托伐他汀对高血糖诱导的小鼠脑缺血后出血转化(HT)的作用及机制。方法36只SPF级雄性C57BL/6小鼠随机分为假手术组、HT模型组和阿托伐他汀组,每组12只。比较各组小鼠神经功能评分、死亡率、HT发生率、HT分级评分,苏木精-伊红染色观察脑组织出血情况,免疫荧光染色评估血脑屏障通透性,Western blot检测缺血半暗带脑组织免疫球蛋白G(IgG)、闭锁连接蛋白1(ZO-1)、闭合蛋白(occludin)、紧密连接蛋白5(claudin5)、基质金属蛋白酶(MMP)2和MMP-9的蛋白表达。结果与假手术组比较,HT模型组神经功能评分、死亡率、HT发生率、HT评分、IgG荧光强度、IgG、MMP-2、MMP-9蛋白表达水平显著增高,ZO-1、occludin、claudin5蛋白表达水平明显降低(P<0.01)。与HT模型组比较,阿托伐他汀组神经功能评分、死亡率、HT发生率、HT评分、IgG荧光强度及IgG、MMP-2、MMP-9蛋白表达水平显著降低[(2.73±1.19)分vs(3.91±0.94)分,16.7%vs 41.6%,58.3%vs 91.6%,(1.00±1.04)分vs(2.58±1.13)分,(504.30±105.52)a.u vs(859.91±153.28)a.u,4.55±1.40 vs 12.06±3.73,1.87±0.41 vs 2.95±0.68,1.47±0.24 vs 2.12±0.23,P<0.05,P<0.01],ZO-1、occludin、claduin5蛋白表达显著升高(1.55±0.20 vs 0.53±0.10,0.92±0.11 vs 0.35±0.07、0.58±0.04 vs 0.30±0.05,P<0.01)。结论阿托伐他汀可通过抑制MMP-2、MMP-9激活,上调ZO-1、occludin、claudin5表达,降低血脑屏障通透性,从而抑制高血糖诱导的脑缺血后HT。展开更多
文摘The changes of blood-brain barrier(BBB)permeability following brain injury werestudied quantitatively by using colloidal gold(CG)particles of various sizes as tracers in 57 rab-bits.In addition,water content in brain tissues was determined.The brain-injured rabbits re-ceived intravenous injection of anisodamine in a dose of 0.3 mg/kg BW at 5rain or 3h after braininjury,and the effect of anisodamine on aherations of BBB permeability and water content of thebrain tissue after brain injury was investigated.The results indicated that an increase of BBBpermeability began at 30min after injury with only a few of 5nm CG tracers present in the endo-cytic pits and endothelial microvilli,and there were 10nm CG tracers passing through the BBB at3 h after brain injury.The increase of BBB permeability reached its peak at 6 h after brain in-jury.More 15nm CG tracers penetrated the BBB by way of pinocytotic vesicule transportationand opening of tight junctions between endothelial cells.The water content in the brain tissueincreased,which was closely correlated to the above-mentioned EBB permeability and giving ad-vantages to the treatment of traumatic brain edema in the present study.
文摘目的探讨长链非编码RNA(lncRNA)-N1LR在脑缺血再灌注损伤后血脑屏障的作用机制。方法原代小鼠脑微血管内皮细胞常规培养,经氧糖剥夺/复糖复氧(OGD/R)处理模拟脑缺血再灌注损伤,实验分对照组、OGD组、lncRNA-N1LR过表达组(OGD处理后转染质粒lncRNA-N1LR过表达)、lncRNA-N1LR沉默组(OGD处理后转染质粒lncRNA-N1LR沉默)。采用逆转录聚合酶链反应检测各组中lncRNA-N1LR mRNA、紧密连接蛋白5(claudin-5)及闭合蛋白(occludin)mRNA表达水平;异硫氰酸荧光素-葡聚糖(FITC-dextran)渗透法检测血脑屏障通透性;免疫蛋白印迹法检测claudin-5、occludin蛋白表达。结果与对照组比较,OGD组lncRNA-N1LR mRNA、occludin、claudin-5 mRNA表达水平下降(0.31±0.01 vs 1.00±0.10,0.42±0.03 vs 1.01±0.13,0.38±0.03 vs 1.00±0.15,P<0.05),血脑屏障FITC-dextran通透性明显升高(58.79±3.04 vs 8.87±0.63,P<0.01)。与OGD组比较,lncRNA-N1LR过表达组lncRNA-N1LR mRNA、occludin、claudin-5 mRNA表达水平升高(0.67±0.07 vs 0.31±0.01,0.92±0.02 vs 0.42±0.03,0.70±0.08 vs 0.38±0.03,P<0.05),血脑屏障FITC-dextran通透性降低(41.57±2.43 vs 58.79±3.04,P<0.05)。与OGD组比较,lncRNA-N1LR沉默组lncRNA-N1LR mRNA、occludin、claudin-5 mRNA表达水平降低(0.21±0.02 vs 0.31±0.01,0.31±0.03 vs 0.42±0.03,0.22±0.02 vs 0.38±0.03,P<0.05),血脑屏障FITC-dextran通透性升高(72.34±1.43 vs 58.79±3.04,P<0.05)。结论LncRNA-N1LR上调可能通过降低血脑屏障通透性发挥神经保护作用。
文摘目的探究阿托伐他汀对高血糖诱导的小鼠脑缺血后出血转化(HT)的作用及机制。方法36只SPF级雄性C57BL/6小鼠随机分为假手术组、HT模型组和阿托伐他汀组,每组12只。比较各组小鼠神经功能评分、死亡率、HT发生率、HT分级评分,苏木精-伊红染色观察脑组织出血情况,免疫荧光染色评估血脑屏障通透性,Western blot检测缺血半暗带脑组织免疫球蛋白G(IgG)、闭锁连接蛋白1(ZO-1)、闭合蛋白(occludin)、紧密连接蛋白5(claudin5)、基质金属蛋白酶(MMP)2和MMP-9的蛋白表达。结果与假手术组比较,HT模型组神经功能评分、死亡率、HT发生率、HT评分、IgG荧光强度、IgG、MMP-2、MMP-9蛋白表达水平显著增高,ZO-1、occludin、claudin5蛋白表达水平明显降低(P<0.01)。与HT模型组比较,阿托伐他汀组神经功能评分、死亡率、HT发生率、HT评分、IgG荧光强度及IgG、MMP-2、MMP-9蛋白表达水平显著降低[(2.73±1.19)分vs(3.91±0.94)分,16.7%vs 41.6%,58.3%vs 91.6%,(1.00±1.04)分vs(2.58±1.13)分,(504.30±105.52)a.u vs(859.91±153.28)a.u,4.55±1.40 vs 12.06±3.73,1.87±0.41 vs 2.95±0.68,1.47±0.24 vs 2.12±0.23,P<0.05,P<0.01],ZO-1、occludin、claduin5蛋白表达显著升高(1.55±0.20 vs 0.53±0.10,0.92±0.11 vs 0.35±0.07、0.58±0.04 vs 0.30±0.05,P<0.01)。结论阿托伐他汀可通过抑制MMP-2、MMP-9激活,上调ZO-1、occludin、claudin5表达,降低血脑屏障通透性,从而抑制高血糖诱导的脑缺血后HT。
