国际脑血管病杂志
國際腦血管病雜誌
국제뇌혈관병잡지
INTERNATIONAL JOURNAL OF CEREBROVASCULAR DISEASES
2013年
2期
96-101
,共6页
付蓓蓓%刘煜敏%孔朝红%程仙送
付蓓蓓%劉煜敏%孔朝紅%程仙送
부배배%류욱민%공조홍%정선송
西酞普兰%脑缺血%血管内皮生长因子%神经保护药%疾病模型,动物%大鼠
西酞普蘭%腦缺血%血管內皮生長因子%神經保護藥%疾病模型,動物%大鼠
서태보란%뇌결혈%혈관내피생장인자%신경보호약%질병모형,동물%대서
Citalopram%Brain Ischemia%Vascular Endothelial Growth Factor%Neuroprotective Agents%Disease Models,Animal%Rats
目的 探讨西酞普兰对局灶性脑缺血再灌注大鼠的神经保护作用及其可能机制.方法 75只雄性Sprague-Dawley大鼠随机分为假手术组、生理盐水对照组和西酞普兰干预组,每组25只.线栓法制作大鼠局灶性脑缺血再灌注模型.改良神经功能缺损量表评价大鼠神经功能缺损(每组5只).激光共聚焦技术观察缺血区微血管直径、密度和总面积(每组5只).酶联免疫吸附法检测血浆血管内皮生长因子(vascular endothelial growth factor,VEGF)浓度(每组5只).免疫组织化学染色法(每组5只)和蛋白质印迹法(每组5只)检测缺血脑组织VEGF表达.结果 模型制作后14 d时,西酞普兰干预组神经功能缺损较生理盐水对照组显著改善[(4.39±0.92)分对(6.57±1.13)分,P=0.015].三维共聚焦血管成像显示,西酞普兰干预组毛细血管直径显著性小于生理盐水对照组[(2.93±0.19)μm对(3.56±0.22)μm; P=0.000]；血管密度显著性高于生理盐水对照组[(232.68±12.54)个/0.002 mm3对(176.26±10.87)个/0.002 mm3；P=0.000]；微血管总面积显著性大于生理盐水对照组[(89 154±3 298) μm2/0.002 mm3对(75 368.14±3 519) μm2/0.002 mm3；P=0.000].酶联免疫吸附法显示,西酞普兰干预组血浆VEGF浓度显著性高于生理盐水对照组[(50.35±5.44) pg/ml对(13.75±4.12) pg/ml；P=0.000].免疫组织化学分析显示,西酞普兰干预组缺血区VEGF表达显著性高于生理盐水对照组(P =0.000).蛋白质印迹法显示,西酞普兰干预组缺血脑组织VEGF表达显著性高于生理盐水对照组[(0.94±0.18)对(0.62±0.22)；P=0.006].结论 西酞普兰可显著减轻脑缺血再灌注大鼠的神经功能缺损,其机制可能与VEGF介导的血管发生有关.
目的 探討西酞普蘭對跼竈性腦缺血再灌註大鼠的神經保護作用及其可能機製.方法 75隻雄性Sprague-Dawley大鼠隨機分為假手術組、生理鹽水對照組和西酞普蘭榦預組,每組25隻.線栓法製作大鼠跼竈性腦缺血再灌註模型.改良神經功能缺損量錶評價大鼠神經功能缺損(每組5隻).激光共聚焦技術觀察缺血區微血管直徑、密度和總麵積(每組5隻).酶聯免疫吸附法檢測血漿血管內皮生長因子(vascular endothelial growth factor,VEGF)濃度(每組5隻).免疫組織化學染色法(每組5隻)和蛋白質印跡法(每組5隻)檢測缺血腦組織VEGF錶達.結果 模型製作後14 d時,西酞普蘭榦預組神經功能缺損較生理鹽水對照組顯著改善[(4.39±0.92)分對(6.57±1.13)分,P=0.015].三維共聚焦血管成像顯示,西酞普蘭榦預組毛細血管直徑顯著性小于生理鹽水對照組[(2.93±0.19)μm對(3.56±0.22)μm; P=0.000]；血管密度顯著性高于生理鹽水對照組[(232.68±12.54)箇/0.002 mm3對(176.26±10.87)箇/0.002 mm3；P=0.000]；微血管總麵積顯著性大于生理鹽水對照組[(89 154±3 298) μm2/0.002 mm3對(75 368.14±3 519) μm2/0.002 mm3；P=0.000].酶聯免疫吸附法顯示,西酞普蘭榦預組血漿VEGF濃度顯著性高于生理鹽水對照組[(50.35±5.44) pg/ml對(13.75±4.12) pg/ml；P=0.000].免疫組織化學分析顯示,西酞普蘭榦預組缺血區VEGF錶達顯著性高于生理鹽水對照組(P =0.000).蛋白質印跡法顯示,西酞普蘭榦預組缺血腦組織VEGF錶達顯著性高于生理鹽水對照組[(0.94±0.18)對(0.62±0.22)；P=0.006].結論 西酞普蘭可顯著減輕腦缺血再灌註大鼠的神經功能缺損,其機製可能與VEGF介導的血管髮生有關.
목적 탐토서태보란대국조성뇌결혈재관주대서적신경보호작용급기가능궤제.방법 75지웅성Sprague-Dawley대서수궤분위가수술조、생리염수대조조화서태보란간예조,매조25지.선전법제작대서국조성뇌결혈재관주모형.개량신경공능결손량표평개대서신경공능결손(매조5지).격광공취초기술관찰결혈구미혈관직경、밀도화총면적(매조5지).매련면역흡부법검측혈장혈관내피생장인자(vascular endothelial growth factor,VEGF)농도(매조5지).면역조직화학염색법(매조5지)화단백질인적법(매조5지)검측결혈뇌조직VEGF표체.결과 모형제작후14 d시,서태보란간예조신경공능결손교생리염수대조조현저개선[(4.39±0.92)분대(6.57±1.13)분,P=0.015].삼유공취초혈관성상현시,서태보란간예조모세혈관직경현저성소우생리염수대조조[(2.93±0.19)μm대(3.56±0.22)μm; P=0.000]；혈관밀도현저성고우생리염수대조조[(232.68±12.54)개/0.002 mm3대(176.26±10.87)개/0.002 mm3；P=0.000]；미혈관총면적현저성대우생리염수대조조[(89 154±3 298) μm2/0.002 mm3대(75 368.14±3 519) μm2/0.002 mm3；P=0.000].매련면역흡부법현시,서태보란간예조혈장VEGF농도현저성고우생리염수대조조[(50.35±5.44) pg/ml대(13.75±4.12) pg/ml；P=0.000].면역조직화학분석현시,서태보란간예조결혈구VEGF표체현저성고우생리염수대조조(P =0.000).단백질인적법현시,서태보란간예조결혈뇌조직VEGF표체현저성고우생리염수대조조[(0.94±0.18)대(0.62±0.22)；P=0.006].결론 서태보란가현저감경뇌결혈재관주대서적신경공능결손,기궤제가능여VEGF개도적혈관발생유관.
Objective To investigate the neuroprotective effect of escitalopram on focal cerebral ischemia/reperfusion in rats and its possible mechanisms.Methods Seventy-five male Sprague-Dawley rats were randomly divided into three groups:sham operation,saline control and escitalopram intervention groups (n =25 in each group).A focal cerebral ischemia reperfusion model in rats was induced by the intraluminal suture method.The modified neurological severity scale was used to evaluate neurological deficit in rats (n =5 in each group).Laser confocal technology was used to observe the microvascular diameter,density,and total area in ischemic region (n =5 in each group).Enzyme-linked immunosorbent assay was used to detect the plasma concentration of vascular endothelial growth factor (VEGF) (n =5 in each group).Immunohistochemical staining (n =5 in each group) and Western blotting (n =5 in each group) were used to detect the expression of VEGF in the ischemic brain tissue.Results At day 14 after modeling,the neurological deficit improved more significantly in the escitalopram intervention group than that in the saline control group (4.39 ±0.92 vs.6.57 ± 1.13; P =0.015).The 3D confocal vascular imaging showed that capillary diameter in the escitalopram intervention group was significantly smaller than that in the saline control group (2.93 ± 0.19 μm vs.3.56 ± 0.22 μm; P ＜0.01); the vascular density was significantly higher than that in the saline control group (232.68 ±12.54/0.002 mm3 vs.176.26 ± 10.87/0.002 mm3; P=0.000); the total microvascular area was significantly greater than that in the saline control group (89 154± 3 298 μm2/0.002 mm3 vs.75 368.14± 3 519 μm2/0.002 mm3; P=0.000).Enzyme-linked immunosorbent assay showed that the plasma VEGF concentration in the escitalopram intervention group was significantly higher than that in the saline control group (50.35 ± 5.44 pg/ml vs.13.75 ± 4.12 pg/ml; P =0.000).Immunohistochemical analysis showed that the VEGF expression in ischemic brain tissue in the escitalopram intervention group was significantly higher than that in the saline control group (P =0.000).Western blotting showed that the VEGF expression in ischemic brain tissue in the escitalopram intervention group was significantly higher than that in the saline control group (0.94 ±0.18 vs.0.62 ±0.22; P =0.006).Conclusions Escitalopram may reduce neurological deficit in cerebral ischemia/reperfusion in rats.Its mechanisms may be associated with VEGF-mediated angiogenesis.
