CAJ | 학술논문

目的观察脑缺血预处理对脑缺血再灌注大鼠脑组织胶质纤维酸性蛋白(glial fibrillary acidic protein,GFAP)表达的影响,探讨星形胶质细胞活化在脑缺血耐受中的意义.方法 36只健康雄性Sprague-Dawley大鼠随机分为缺血预处理再缺血组、缺血组和对照组,每组12只,前2组分别在2 h大脑中动脉闭塞(middle cerebral artery occlusion,MCAO)前3 d给予10 min的MCAO预处理或假手术,第2次MCAO后24 h处死,对照组仅给予2次间隔3 d的假手术.比较各组脑梗死体积、组织病理学变化和GFAP表达.结果缺血预处理后再缺血组和缺血组梗死体积分别为(136.85±14.51)mm3和(281.37±29.93)mm3,前者较后者显著缩小53.15%(P=0.007);同时,缺血预处理再缺血组神经元变性坏死显著减轻,并伴有GFAP表达显著上调(2组免疫组化染色平均吸光度分别为102.66±8.39和86.28±6.19,P=0.009).结论缺血预处理可诱导脑缺血耐受,促进GFAP表达,星形胶质细胞活化可能是脑缺血耐受产生的机制之一.
목적 관찰뇌결혈예처리대뇌결혈재관주대서뇌조직효질섬유산성단백(glial fibrillary acidic protein,GFAP)표체적영향,탐토성형효질세포활화재뇌결혈내수중적의의.방법 36지건강웅성Sprague-Dawley대서수궤분위결혈예처리재결혈조、결혈조화대조조,매조12지,전2조분별재2 h대뇌중동맥폐새(middle cerebral artery occlusion,MCAO)전3 d급여10 min적MCAO예처리혹가수술,제2차MCAO후24 h처사,대조조부급여2차간격3 d적가수술.비교각조뇌경사체적、조직병이학변화화GFAP표체.결과 결혈예처리후재결혈조화결혈조경사체적분별위(136.85±14.51)mm3화(281.37±29.93)mm3,전자교후자현저축소53.15%(P=0.007);동시,결혈예처리재결혈조신경원변성배사현저감경,병반유GFAP표체현저상조(2조면역조화염색평균흡광도분별위102.66±8.39화86.28±6.19,P=0.009).결론 결혈예처리가유도뇌결혈내수,촉진GFAP표체,성형효질세포활화가능시뇌결혈내수산생적궤제지일.
Objective To observe the effect of focal cerebral ischemic preconditioning on the expression of glial fibrillary acidic protein (GFAP) and to investigate the significance of astrocyte activation in cerebral ischemic tolerance.Methods Thirty-six healthy male SpragueDawley rats were randomly divided into reischenmic,ischemic and control groups (n = 12 in each group) after ischemic preconditioning.The former two groups received 10 minutes middle cerebral artery occlusion (MCAO) preconditioning or sham operation 3 days before the 2-hour MCAO.The rats were killed 24 hours after the second MCAO.The control group only receivedthe two sham operations with an interval of three days.The infarct volume,histopathological changes,and GFAP expression in each group were compared.Results The infarct volume after ischemic preconditioning in the reischenmic and ischemic groups was 136.85 ± 14.51 mm3and 281.37 ± 29.93 mm3 respectively.The former was significantly reduced 53.15%compared to the latter (P =0.007).At the same time,neuronal degeneration and necrosis was reduced significantly,and GFAP expression was upregulated significantly (the mean absorbance for immunohistochemical staining in both groups was 102.66 ± 8.39 and 86.28 ± 6.19respectively,P = 0.009) after ischemic preconditioning in the reischemic group.Conclusions Focal ischemic preconditioning may induce brain ischemic tolerance and promote GFAP expression.The activation of astrocytes may be one of the mechanisms of cerebral ischemic tolerance.