摘要
目的探讨促血小板生成素对大鼠局灶性脑缺血再灌注损伤后的保护作用及机制。方法采用线栓法阻断大鼠大脑中动脉血流制成局灶性脑缺血再灌注损伤模型。将60只雄性SD大鼠随机分成促血小板生成素(TPO)组、缺血再灌注组、假手术组和正常组。于缺血开始时TPO组给予TPO 5μg/kg腹腔注射;缺血再灌注组给予等剂量生理盐水。分别于再灌注6、12、24、48 h后断头取脑、切片,进行HE染色、Bcl-2免疫组化染色和细胞凋亡检测。结果缺血再灌注后,TPO组和缺血再灌注组大鼠缺血侧皮层可检测到凋亡细胞,且TPO组凋亡细胞数明显少于缺血再灌注组,差异有统计学意义(P<0.05),而假手术组及正常组未检测到凋亡细胞;TPO组和缺血再灌注组缺血侧皮层Bcl-2阳性细胞数均高于假手术组及正常组,与缺血再灌注组相比,TPO组Bcl-2蛋白表达显著增高,差异有统计学意义(P<0.05)。结论 TPO可抑制缺血再灌注损伤后缺血侧皮层的细胞凋亡,其机制可能是通过上调Bcl-2基因表达而实现。
Objective To study the protective effects and the mechanism of thrombopoietin （TPO） on cerebral ischemia-reperfusion in rats. Methods Thread embolism was performed to establish cerebral ischemia-reperfusion model in rats. Sixty SD rats were divided into TPO group, ischemia-reperfusion group, sham-operation group and normal group randomly. The TPO was given to TPO group at the beginning of ischemia at a dose of 5 μg/kg; Ischemia -reperfusion group was given isodose physiological saline. 6 h, 12 h, 24 h and 48 h after reperfusion, the rats were executed and the brain tissues were cut into sections for HE staining and theimmunohistochemieal staining to detect Bcl-2 and apoptosis. Results After ischemia-reperfusion, the apoptotic cells were detected in TPO group and ischemia-reperfusion group in lateral cortex of rats, and the apoptosis cell number of TPO group was obviously less than that of ischemia-reperfusion group （P〈0. 05）. While no apoptotic cells were detected in sham-operation group and normal group. The number of Bcl-2 positive cells in TPO group and ischemia-reperfusion group was higher than that in control group and normal group. Expression of Bcl-2 protein in TPO group was significantly higher than that in ischemia-reperfusion group （ P〈 0. 05 ）. Conclusions TPO can inhibit cell apoptosis of ischemia lateral cortex after ischemia-reperfusion injury, and the mechanism may be through raising the expression of Bcl-2 genes.
出处
《实用老年医学》
CAS
2014年第1期46-48,共3页
Practical Geriatrics
