电针对大鼠局灶性脑缺血脑内Calbindin-D28k表达的影响

目的 :探讨钙结合蛋白家族成员Calbindin D2 8k与电针抗缺血性脑损伤的关系。方法 :用改良线栓法制备SD大鼠大脑中动脉 (MCA)阻塞 再灌注模型 ,应用TTC及HE组织化学染色观察缺血及电针后梗塞灶的变化 ,并应用免疫组织化学方法对大鼠局灶性脑缺血组织内Calbindin D2 8k免疫阳性细胞的分布及电针对该分布的影响进行观察。结果 :电针可明显改善局灶性脑缺血所造成的神经缺损体征 ;但缺血组及电针组Calbindin D2 8k免疫阳性细胞在梗塞灶中心区几乎检测不出 ,缺血组在半影区与对照组相比表达上调 (P <0 0 5 ) ;电针组Calbindin D2 8k在半影区的表达与缺血组之间差异无显著性意义 (P >0 0 5 )。结论 :局灶性脑缺血对Calbindin D2 8k在半影区反应性表达增强可能用以缓冲胞内过多的游离钙 ;电针在脑缺血时对神经元具有保护效应 ,但可能并不是通过调整Calbindin D2 8k的表达而实现的

Effect of Electroacupuncture on Expression of Calbindin-D28k in the Brain in Rats of Focal Cerebral Ischemia

Purpose To study on relation of the expression of Calbindin D 28k to anti ischemia cerebral injuries of electroacupuncture(EA). Methods In the rat model of reversible meddle cerebral artery occlusion(rMCAO) for 30 min with reperfusion 48 hours, pathological changes of the infarction area were observed by HE staining, and the expression of Calbindin D 28k in different brain areas were investigated with immunohistochemical staining methods, and the influence of EA was observed. Results EA can obviously improve the symptoms of nerve deficiency induced by local cerebral ischemia; and in the ischemic group and the EA group positive immunoreactive neurons of Calbindin D 28k are scarely; observed in the infarction core. However in penumbra the expression of Calbindin D 28k in the ischemic group increased as compared with the control group( P <0 05), but there is no significant difference in the expression in penumbra between the EA group and the ischemic group ( P >0 05). Conclusion The expression of Calbindin D 28k in the penumbra in focal cerebral ischemia increases, and EA has protective action on neurons, but this is not be carried out through regulating Calbindin D 28k expression.