河北北方学院学报(自然科学版)
河北北方學院學報(自然科學版)
하북북방학원학보(자연과학판)
JOURNAL OF HEBEI NORTH UNIVERSITY(NATURAL SCIENCE EDITION)
2013年
4期
59-62
,共4页
丹参酚酸B盐%黄芪多糖%预处理%凋亡%胶质纤维酸性蛋白%大脑中动脉梗塞模型%缺血再灌注
丹參酚痠B鹽%黃芪多糖%預處理%凋亡%膠質纖維痠性蛋白%大腦中動脈梗塞模型%缺血再灌註
단삼분산B염%황기다당%예처리%조망%효질섬유산성단백%대뇌중동맥경새모형%결혈재관주
salvianolic acid B%astragalus polysacharin%preconditioning%apoptosis%glial fibrillary acidic protein%middle cerebral artery occlusion%ischemia/reperfusion
目的观察丹参酚酸B盐联合黄芪多糖预处理对 SD大鼠脑缺血再灌注损伤细胞凋亡及脑组织中胶质纤维酸性蛋白(GFAP)表达的影响,探讨该预处理方式对脑缺血再灌注损伤后梗死灶及缺血半暗带重塑的影响。方法以线栓法建立缺血再灌注模型---大脑中动脉梗塞模型(MCAO)。将138只雄性 SD大鼠随机分为6组(各23只):正常组、假手术组、模型(缺血再灌注)组、丹参酚酸B盐组、黄芪多糖预处理组及丹参酚酸B盐联合黄芪多糖预处理组。观察丹参酚酸 B盐联合黄芪多糖预处理对大鼠脑缺血再灌注神经功能、脑梗死面积和病理形态学的影响。采用TUNEL法检测缺血半暗带和灶中心区凋亡细胞,采用免疫组化法检测缺血半暗带和灶中心区 GFAP表达的变化。结果模型组与假手术组相比,缺血半暗带凋亡细胞及 GFAP阳性细胞数目增多;丹参酚酸 B盐联合黄芪多糖预处理可不同程度地降低实验性脑缺血大鼠的神经功能评分(Longa评分)、减小梗死灶面积并使脑组织病理形态改变减轻(P<0.05);丹参酚酸B盐联合黄芪多糖预处理组大鼠脑组织缺血半暗带凋亡细胞和 GFAP表达减少,而梗死灶中心凋亡细胞和 GFAP表达却增多。结论丹参酚酸B盐联合黄芪多糖预处理可能通过调节脑缺血再灌注损伤细胞凋亡和 GFAP表达而促进脑重塑。
目的觀察丹參酚痠B鹽聯閤黃芪多糖預處理對 SD大鼠腦缺血再灌註損傷細胞凋亡及腦組織中膠質纖維痠性蛋白(GFAP)錶達的影響,探討該預處理方式對腦缺血再灌註損傷後梗死竈及缺血半暗帶重塑的影響。方法以線栓法建立缺血再灌註模型---大腦中動脈梗塞模型(MCAO)。將138隻雄性 SD大鼠隨機分為6組(各23隻):正常組、假手術組、模型(缺血再灌註)組、丹參酚痠B鹽組、黃芪多糖預處理組及丹參酚痠B鹽聯閤黃芪多糖預處理組。觀察丹參酚痠 B鹽聯閤黃芪多糖預處理對大鼠腦缺血再灌註神經功能、腦梗死麵積和病理形態學的影響。採用TUNEL法檢測缺血半暗帶和竈中心區凋亡細胞,採用免疫組化法檢測缺血半暗帶和竈中心區 GFAP錶達的變化。結果模型組與假手術組相比,缺血半暗帶凋亡細胞及 GFAP暘性細胞數目增多;丹參酚痠 B鹽聯閤黃芪多糖預處理可不同程度地降低實驗性腦缺血大鼠的神經功能評分(Longa評分)、減小梗死竈麵積併使腦組織病理形態改變減輕(P<0.05);丹參酚痠B鹽聯閤黃芪多糖預處理組大鼠腦組織缺血半暗帶凋亡細胞和 GFAP錶達減少,而梗死竈中心凋亡細胞和 GFAP錶達卻增多。結論丹參酚痠B鹽聯閤黃芪多糖預處理可能通過調節腦缺血再灌註損傷細胞凋亡和 GFAP錶達而促進腦重塑。
목적관찰단삼분산B염연합황기다당예처리대 SD대서뇌결혈재관주손상세포조망급뇌조직중효질섬유산성단백(GFAP)표체적영향,탐토해예처리방식대뇌결혈재관주손상후경사조급결혈반암대중소적영향。방법이선전법건립결혈재관주모형---대뇌중동맥경새모형(MCAO)。장138지웅성 SD대서수궤분위6조(각23지):정상조、가수술조、모형(결혈재관주)조、단삼분산B염조、황기다당예처리조급단삼분산B염연합황기다당예처리조。관찰단삼분산 B염연합황기다당예처리대대서뇌결혈재관주신경공능、뇌경사면적화병리형태학적영향。채용TUNEL법검측결혈반암대화조중심구조망세포,채용면역조화법검측결혈반암대화조중심구 GFAP표체적변화。결과모형조여가수술조상비,결혈반암대조망세포급 GFAP양성세포수목증다;단삼분산 B염연합황기다당예처리가불동정도지강저실험성뇌결혈대서적신경공능평분(Longa평분)、감소경사조면적병사뇌조직병리형태개변감경(P<0.05);단삼분산B염연합황기다당예처리조대서뇌조직결혈반암대조망세포화 GFAP표체감소,이경사조중심조망세포화 GFAP표체각증다。결론단삼분산B염연합황기다당예처리가능통과조절뇌결혈재관주손상세포조망화 GFAP표체이촉진뇌중소。
Objective To observe the impacts of salvianolic acid B (SA-B) combined astragalus po-lysacharin (aps)preconditioning on apoptosis of neuronal cells and expression of GFAP after focal cere-bral ischemia-reperfusion,while investigating the effects on remodeling in ischemic penumbra and ischemic focus center.Methods The string-fastening method was used to establish focal ischemia-reperfusion mod-els in SD rats and one hundred and thirty-eight SD male rats were randomly divided into six groups:nor-mal (n=23),shamop-erated group (n=23),model (ischemia and reperfusion)group (n=23),salvianolic acid B (SA-B ) preconditioning group (n=23),astragalus polysacharin (aps ) preconditioning group (n=23),salvianolic acid B (SA-B ) combined astragalus polysacharin (aps ) preconditioning group (n=23).The effects of salvianolic acid B (SA-B) combined astragalus polysacharin (aps) precondition-ing were observed on neuralogical function,area of cerebral infarction and pathomorphology of brain tis-sues,after focal cerebral ischemia-reperfusion.The method of TUNEL was used to measure level of ap-optosis of neuronal cells,and immunohistochemistry was used to measure level of expression of GFAP in ischemic penumbra and ischemic focus center.Results In the model group,the number of apoptosis of neuronal cells and expression of GFAP increased markedly in ischemic penumbra compared with that in sham-operated group,the score of neurological function of experimental cerebral ischemia rat and area of cerebral infarction were decreased to various degrees, and degree of pathomorphological change of brain tissues was lessened in salvianolic acid B (SA-B)combined astragalus polysacharin (aps)preconditioning group (P<0.05).The apoptosis of neuronal cells and expression of GFAP were less in ischemic penum-bra.Meanwhile,the apoptosis of neuronal cells and expression of GFAP increased in infarction area in salvianolic acid B (SA-B)combined astragalus polysacharin (aps)preconditioning group.Conclusion salvianolic acid B (SA-B) combined astragalus polysacharin (aps) preconditioning could promote the is-chemic neuron to revive and become more plastic by regulating apoptosis of neuronal cells and expression of GFAP after focal cerebral ischemia-reperfusion.