摘要
目的观察糖原合成酶激酶3β(glycogen synthase kinase-3β,GSK-3β)及Bax在脑缺血再灌注损伤EPO干预中的变化,探讨促红细胞生成素(EPO)对大鼠缺血再灌注损伤的作用。方法采用血管阻断法制作大鼠单侧(左)脑缺血再灌注模型。将54只SD大鼠随机分为正常组6只、缺血再灌注组24只和EPO治疗组24只,观察时相点为缺血后6、12、24、48h,观察脑组织含水量变化,HE染色进行脑组织病理观察及细胞计数,TUNEL法检测海马区细胞凋亡变化,免疫组织化学染色及WB法观察GSK-3β和Bax的表达变化。结果EPO组病理变化较对照组轻,脑组织含水量较对照组显著减少,EPO组缺血24h及48h平均脑组织细胞数显著多于对照组、TUNEL阳性细胞数量显著少于对照组。EPO组GSK-3β和Bax免疫组化染色阳性细胞数量明显下降,蛋白水平显著下降。结论EPO能有效抑制大鼠脑缺血再灌注后脑组织水肿及细胞凋亡发生,可能与其使GSK-3β和Bax活性的降低有关。
Objective To investigate the changes and effect of glycogen synthase kinase-3β（GSK-3β） and Bax on the erythropoietin（EPO） intervention on the rat brain injury suffered from ischemia-reperfusion. Methods The rat model of ischemia-reperfusion was established with middle cerebral artery occlusion. The rats were treated with ischemic injury for 2h, then given rhEPO （2 000u/kg） or saline,i, p, The brain was removed at different time after operation （6,12,24,48h） to make paraffin sections. HE staining and TUNEL staining detected the death of neurons in hippocampus. The expression of GSK-3β and Bax were detected by immunohistochemistry staining and Western blotting（WB）. Results The pathological changes of the EPO group were lighter than that of the control group. The water content ratio in the EPO group was less than that in the control group. The cell number was more and the positive TUNEL cells were less in the EPO group. The positive cell number and expression level of GSK-3β and Bax were less than those in the control group. Conclusion EPO alleviates neurons apoptosis in hippocampi region in rats suffered from ischermia-reperfusion injury. The protection role of EPO is related to the decreasing of GSK-3β and Bax.
出处
《重庆医学》
CAS
CSCD
2007年第16期1629-1631,共3页
Chongqing medicine
