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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(diabetesmellitus,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(glialfibrillaryacidicprotein,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(3d时IR,DM/IR组:75±6,96±70)及GFAP阳性细胞数(3d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。
Objective: To explore the mechanism of endothelin-3 and astrocyte in cerebral ischemia-reperfusion injury in diabetic mice. Methods: Sixty-six adult male Kunming mice were randomly divided into five groups according to random number table: diabetes mellitus (DM) group (n = 6), diabetic mellitus / ischemia-reperfusion (DM / IR group (n = 24), ischemia-reperfusion group (n = 24), sham operation group (n = 6) and normal control group (n = 6). The amount of endothelin-3 and glial fibrillary acidic protein (glial fibrillary acid protein, GFAP) were detected by immunohistochemistry in the frontal cortex of mice. Results: A small amount of endothelin-3 was seen in the frontal and parietal cortex of mice in the control group, while GFAP positive cells were scattered in the control group. Endothelins-3 positive neurons in diabetic group (IR, DM / IR group: 75 ± 6,96 ± 70) and GFAP positive cells (IR, DM / IR group at 3d: 687 ± 17,702 ± 35) were significantly higher than those in control group (endothelin -3: 28 ± 9; GFAP: 183 ± 11) P <0.01). Conclusion: Diabetes mellitus is one of the important factors of cerebral ischemia-reperfusion injury. Endothelin-3 and astrocyte activation may be one of the mechanisms of aggravating neuronal injury in diabetic mice.