摘要
目的 研究促红细胞生成素 (erythropoietin ,rhEPO)在大鼠局灶性脑缺血再灌注损伤中对Caspase - 3蛋白的影响 ,探讨rhEPO的脑保护机制。 方法 线栓法建立大鼠局灶性脑缺血再灌注损伤模型 ,NISS染色观察缺血半暗区的病理形态变化 ,免疫组织化学方法检测活化的Caspase - 3的表达 ,TTC染色观察缺血损伤面积。结果 Caspase - 3阳性细胞在对照组脑组织内散在分布 ,缺血组和治疗组在大脑皮层较为密集。缺血组阳性细胞数显著高于对照组 (P<0 .0 1) ,治疗组阳性细胞数显著低于缺血组 (P <0 .0 1)。结论 Caspase- 3在大鼠局灶性脑缺血再灌注中活性显著增高 ,rhEPO能有效抑制Caspase - 3激活 ,从而抑制大鼠局灶性脑缺血再灌注损伤中缺血损伤及细胞凋亡 。
Objective To explore the adjustive effect on Caspase-3 of rhEPO after focal ischemia and reperfusion in rats, and reveal the mechanism of neuro-protection by rhEPO. Methods The acute focal cererbral ischemia/reperfution model was established with suture emboli as described by Nagasawa. The brain tissues were used to make the freeze-sections. Some sections were used for the observation of neuron pathologic change in by NISS staining, others for immunohisochemistry to detect the expression of Caspase-3 in ischemia semi-dim region. Counted the amount of positive cells and analyzed the result. Another 24 rats were killed at 48h after reperfusion for TTC staining. Results The positive stained cells were distributed dispersively in normal group and sham group, and more intensively in cerebral cortex of the other two groups. In semi-dim region, the amount of positive cells in ischemia and reperfusion group, was significant larger than in control sham group (P<0.01) and rhEPO group (P<0.01). Conclusions The activation of caspase-3 in rats which were focal cerebral ischemia and reperfusion operated was striking, and rhEPO could Inhibit this activation significantly. It indicated that rhEPO might be one of protective drugs for ischemia’s effective therapy.
出处
《神经疾病与精神卫生》
2004年第5期337-340,共4页
Journal of Neuroscience and Mental Health
