天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2013年
12期
1177-1179
,共3页
刘瑞%高维娟%钱涛%王利%董雅洁%董贤慧
劉瑞%高維娟%錢濤%王利%董雅潔%董賢慧
류서%고유연%전도%왕리%동아길%동현혜
再灌注损伤%黄芪%海马%细胞凋亡%细胞凋亡蛋白酶激活因子1
再灌註損傷%黃芪%海馬%細胞凋亡%細胞凋亡蛋白酶激活因子1
재관주손상%황기%해마%세포조망%세포조망단백매격활인자1
reperfusion injury%astragalus membranaceus%hippocampus%apoptosis%Apaf-1
目的:观察黄芪注射液对脑缺血再灌注大鼠海马神经元形态学和Apaf-1表达的影响。方法 SD大鼠随机分为假手术组、脑缺血再灌注组(再灌注组)和黄芪注射液处理组(实验组)。采用Pulsinelli四血管阻断法建立大鼠脑缺血再灌注模型,实验组于术前30 min腹腔注射黄芪注射液6 mL/kg,每24 h注射1次,各组于再灌注后24 h断头取脑。采用HE染色,光镜下观察海马组织病理学改变;透射电镜下观察海马神经元超微结构变化;免疫组织化学法和Western blot法检测大鼠海马组织凋亡蛋白酶激活因子-1(Apaf-1)蛋白表达的变化。结果与假手术组比较,再灌注组大鼠海马神经元出现胞核及线粒体损伤,并且Apaf-1蛋白的表达明显升高(免疫组化:0.024±0.001 vs 0.109±0.011;Western blot法:0.270±0.018 vs 0.894±0.072,均P<0.01),与再灌注组比较,实验组大鼠海马神经元胞核及线粒体损伤明显减轻,而Apaf-1蛋白的表达明显降低(免疫组化:0.048±0.005;Western blot法:0.392±0.046,均P<0.01)。结论黄芪注射液可减轻脑缺血再灌注大鼠海马神经元的损伤,其作用机制可能与抑制Apaf-1蛋白表达有关。
目的:觀察黃芪註射液對腦缺血再灌註大鼠海馬神經元形態學和Apaf-1錶達的影響。方法 SD大鼠隨機分為假手術組、腦缺血再灌註組(再灌註組)和黃芪註射液處理組(實驗組)。採用Pulsinelli四血管阻斷法建立大鼠腦缺血再灌註模型,實驗組于術前30 min腹腔註射黃芪註射液6 mL/kg,每24 h註射1次,各組于再灌註後24 h斷頭取腦。採用HE染色,光鏡下觀察海馬組織病理學改變;透射電鏡下觀察海馬神經元超微結構變化;免疫組織化學法和Western blot法檢測大鼠海馬組織凋亡蛋白酶激活因子-1(Apaf-1)蛋白錶達的變化。結果與假手術組比較,再灌註組大鼠海馬神經元齣現胞覈及線粒體損傷,併且Apaf-1蛋白的錶達明顯升高(免疫組化:0.024±0.001 vs 0.109±0.011;Western blot法:0.270±0.018 vs 0.894±0.072,均P<0.01),與再灌註組比較,實驗組大鼠海馬神經元胞覈及線粒體損傷明顯減輕,而Apaf-1蛋白的錶達明顯降低(免疫組化:0.048±0.005;Western blot法:0.392±0.046,均P<0.01)。結論黃芪註射液可減輕腦缺血再灌註大鼠海馬神經元的損傷,其作用機製可能與抑製Apaf-1蛋白錶達有關。
목적:관찰황기주사액대뇌결혈재관주대서해마신경원형태학화Apaf-1표체적영향。방법 SD대서수궤분위가수술조、뇌결혈재관주조(재관주조)화황기주사액처리조(실험조)。채용Pulsinelli사혈관조단법건립대서뇌결혈재관주모형,실험조우술전30 min복강주사황기주사액6 mL/kg,매24 h주사1차,각조우재관주후24 h단두취뇌。채용HE염색,광경하관찰해마조직병이학개변;투사전경하관찰해마신경원초미결구변화;면역조직화학법화Western blot법검측대서해마조직조망단백매격활인자-1(Apaf-1)단백표체적변화。결과여가수술조비교,재관주조대서해마신경원출현포핵급선립체손상,병차Apaf-1단백적표체명현승고(면역조화:0.024±0.001 vs 0.109±0.011;Western blot법:0.270±0.018 vs 0.894±0.072,균P<0.01),여재관주조비교,실험조대서해마신경원포핵급선립체손상명현감경,이Apaf-1단백적표체명현강저(면역조화:0.048±0.005;Western blot법:0.392±0.046,균P<0.01)。결론황기주사액가감경뇌결혈재관주대서해마신경원적손상,기작용궤제가능여억제Apaf-1단백표체유관。
Objective To investigate the effects of astragalus injection on the morphology and expression of Apaf-1 in hippocampal neurons after cerebral ischemia reperfusion in rats. Methods The male SD rats were randomly divided into 3 groups, sham-operated group, cerebral ischemia-reperfusion group (reperfusion group) and astragalus injection interven-tion group (experiment group). The global cerebral ischemia-reperfusion rat model was established by Pulsinelli four-vessel occlusion method. The astragalus injection group was intraperitoneally injected with astragalus 6 mL/kg, 30 mins before sur-gery and repeated every 24 h. Rat brains were removed 24 h after reperfusion in each group. HE staining was used to observe the pathological changes of the hippocampal neurons under the light microscope. The ultrastructural changes of hippocam-pal neurons were observed by transmission electron microscopy. Immunohistochemistry and Western blot methods were used to measure the expression of apoptotic protease activating factor-1(Apaf-1) protein. Results Compared with sham-operat-ed group, nuclear and mitochondrial damage was found in reperfusion group, and the expression of Apaf-1 protein increased obviously in hippocampus(Immunohistochemistry result:0.024 ± 0.001 vs 0.109 ± 0.011;Western blot result:0.270 ± 0.018 vs 0.894±0.072, P<0.01). Compared with reperfusion group, the damage in nuclear and mitochondria was relieved obviously in experiment group, and the expression of Apaf-1 protein in hippocampus was significantly decreased (Immunohistochemistry result:0.048±0.005;Western blot result:0.392±0.046, P<0.01). Conclusion Astragalus injection can reduce pathological damage of hippocampal neurons after cerebral ischemia and reperfusion in rats, and the mechanism is related with inhibiting of Apaf-1 protein.