2型糖尿病小鼠脑缺血再灌注额顶叶皮质因子变化及神经症状观察

目的探讨内皮素-3和星形胶质细胞在糖尿病小鼠脑缺血再灌注损伤中的作用机制. 方法将 66只成年雄性昆明小鼠按随机数字表法分为 5组单纯糖尿病(diabetes mellitus,DM)组 (n=6),糖尿病合并脑缺血再灌注( diatetesmellitus/ischemia-reperfusion,DM/IR)组( n=24),脑缺血再灌注(ischemia-reperfusion,IR)组( n=24),假手术组( n=6),正常对照组( n=6).分别取小鼠额顶叶皮质进行免疫组化染色检测内皮素-3和胶质纤维酸性蛋白( glial fibrillary acidic protein,GFAP)的表达. 结果对照组小鼠额叶、顶叶皮质Ⅲ-Ⅵ层可见少量内皮素-3、 GFAP阳性细胞散在分布 ;糖尿病组内皮素- 3阳性神经元( 3 d时 IR,DM/IR组 75± 6, 96± 70)及 GFAP阳性细胞数( 3 d时 IR, DM/IR组 687± 17, 702±35)均比对照组(内皮素- 3 28± 9; GFAP 183± 11)明显增多 (P< 0.01). 结论糖尿病是脑缺血再灌注损伤重要因素之一;内皮素-3和星形胶质细胞激活可能是糖尿病小鼠神经细胞损伤加重恶化的机制之一.

Changes of endothelin-3 in the cortex of the frontal and parietal lobes of type 2 diabetic mice following ischemia-reperfusion and observation of neurological symptoms

AIM:To explore the role of endothelin(ET)-3 and astrocytes in cerebral ischemia-reperfusion injury in diabetic mice. METHODS:A total of 66 adult male Kunming mice were randomly divided into diabetes mellitus group(DM group,n=6),diabetes mellitus with cerebral ischemia-reperfusion group(DM/IR group,n=24),cerebral ischemia-reperfusion group(IR group,n=24),sham operation group(SO group,n=6) and control group(n=6).The expressions of ET-3 and glial fibrillary acidic protein(GFAP) in the cortex of the frontal and parietal lobes of the mice were examined immunohistochemically. RESULTS:In the control group,a small amount of ET-3 expressed in the ⅢⅣ layers of the frontal and parietal lobe cortex in mice,with scattered GFAP-positive cells.On the third day of reperfusion,the number of ET-3-positive neurons and GFAP-positive cells was 75± 6 and 96± 70 respectively in the IR group,and 687± 17 and 702± 35 in the DM/IR group,both higher than those of the control group (28± 9 and 183± 11 respectively,P< 0.01). CONCLUSION:Diabetes is one of the important causes of cerebral ischemia-reperfusion injury,and ET-3 and activated astrocytes may worsen the neural injuries in diabetic mice.