摘要
目的探讨小鼠脑缺血/再灌注后胶质细胞形态学与数量的变化及其临床意义。方法采用随机方法将32只健康昆明雄性小鼠分为假手术组和模型组,每组16只。制备脑缺血/再灌注损伤模型,应用免疫组织化学方法分别标记星形胶质细胞特异性蛋白胶质纤维酸性蛋白(glial fibrillary acidic protein,GFAP)与小胶质细胞特异性蛋白离子钙接头蛋白抗体(ionized calcium-binding adaptor molecule 1,Iba-1),观察脑缺血/再灌注小鼠海马区胶质细胞形态及数量的变化。结果脑缺血/再灌注损伤后模型组小鼠海马区锥体细胞排列紊乱,细胞脱失明显,细胞核体积变小,深染,呈核固缩。GFAP与Iba-1阳性细胞在形态上表现为胞体肥大,分支变粗;模型组阳性细胞数分别为(12.56±1.58)个/HP和(9.63±1.50)个/HP,均显著多于假手术组,差异具有统计学意义(P<0.01)。结论小鼠局灶性脑缺血/再灌注损伤后海马区胶质细胞过度活化,可能参与加重脑缺血/再灌注后组织损伤及神经元凋亡。
Objective To observe the effects of ischemia/reperfusion on the morphology and numbers of glia cell in the mice brain and study the mechanism of gial cells in the ischemia/reperfusion injury.Methods 32 male mice were randomly divided into two groups: sham group(n=10) and model group(n=10).Using the mice model of cerebral ischemia-reperfusion injury,the expression of astrocyte-specific glial fibrillary acidic protein(GFAP) and micrglia-specific ionized calcium-binding adapter molecule-1(Iba-1) were detected by immunohistochemistry to observe the morphology of gial cell.Results The levels of GFAP and Iba-1 were successively increased(P<0.05),in the model group compared with those in the sham group.Conclusion The present study provides the in vivo evidence that cerebral ischemic/reperfusion injury could have enhanced the activation of glia cells.The injury mechanism is related to affect the morphology and activation of glia cells.
出处
《新疆医科大学学报》
CAS
2012年第2期158-162,共5页
Journal of Xinjiang Medical University
基金
国家自然科学基金(81060104)
