摘要
目的比较脑脉通联合不同时间窗溶栓治疗对脑缺血大鼠神经细胞凋亡的阻抑作用及其对相关调控基因的影响。方法大鼠随机分为假手术组、模型组、尿激酶溶栓组(简称溶栓组)、脑脉通组、脑脉通+尿激酶溶栓组(简称联合组)。自体血栓结合线栓阻塞大鼠大脑中动脉制备血栓栓塞性脑缺血动物模型。大鼠分别于缺血后3、6、9 h经导管由区域动脉进行溶栓。动脉给药后24 h,观察大鼠脑组织神经细胞凋亡变化；测定细胞凋亡相关基因蛋白bax、caspase-3和bcl-2表达变化。结果各模型组大鼠TUNEL阳性细胞均较假手术组增多、bax和caspase-3表达增强、bcl-2表达下调；与模型组比较,各用药组大鼠TUNEL阳性细胞数减少,溶栓组、联合组各时间点bax和caspase-3表达减弱、bcl-2表达上调；各组6 h和9 h较其3 h TUNEL阳性细胞数增加、bax和caspase-3表达增强、bcl-2表达下调；除脑脉通组外各组9 h较6 h组TUNEL阳性细胞数增多、bax和caspase-3表达增强,bcl-2减弱；联合组较单一用药组TUNEL阳性细胞数减少、6 h和9 h组bax及caspase-3表达减弱、bcl-2增强。结论脑缺血损伤可引起促凋亡基因表达上调和抑凋亡基因表达下调,神经细胞凋亡发生,该变化随缺血时间延长而显著；脑脉通及溶栓治疗均可阻抑脑缺血神经细胞凋亡,但以二者联合用药的效果尤为理想,通过下调促凋亡基因bax和caspase-3表达、上调抑凋亡基因bcl-2的表达对神经细胞凋亡发挥阻抑作用。
Objectives To compare depression effects of Naomaitong associated thrombolysis using at different time windows through artery on neurocyte apoptosis and its correlated controlling gene in rats with thrombus - occluded cerebral ischemia. Methods Rats were randomly divided into sham - operated group, model group, UK group（ abbreviated as thrombolysis group）, Naomaitong group, UK adds Naomaitong group （ abbreviated as association group）. Thrombus - occluded cerebral ischemia model group was duplicated by autologous blood blot and inserted nylon thread. Rats were administrated with thrombolysis therapy through artery at 3,6 ,and 9 h after cererbral ischemia. At 24 h of administration through artery, brain neurocyte apoptosis （TUNEL cell number） of rats was observed, and expression of bax, caspase- 3 and bcl -2 were measured, Results Compared with sham -operated group, TUNEL cell numbers and expression of bax, caspase - 3 increased in model group, while expression of bcl - 2 decreased. TUNEL cell nunlbers in each administration group decreased and expression of bax, caspase -3 in each thrombolysis group and association group, while expression of bcl - 2 up regulated, these changes appeared more significant in 3 h group than that in 9 h and 6 h group. In comparison with each simple administration group, TUNEL cell numbers in association group reduced, and expression of bax, caspase-3 in 9 h and 6 h group attenuated ,while expression of bcl-2 up regulated. Conclusion Up regulation of expression in promoting apoptosis and down regulation of expression in inhibating apoptosis could be caused by injury of cerebral ischemia and the changes became more obviously following the prolonging of ischemia time. Naomaitong and thrombolysis could inhibate apoptosis caused by cerebral ischemia, but effects of their association appeared more significant. Association of Naomaitong and thrombolysis could inhibate apoptosis by up regulating expression of bax and caspase - 3, as well as down regulating expression of bcl - 2.
出处
《中国急救医学》
CAS
CSCD
北大核心
2007年第1期39-41,共3页
Chinese Journal of Critical Care Medicine
基金
国家自然科学基金(No.C03050311)
河南省高校创新人才培养基金(No.2000-10)
关键词
脑缺血
大鼠
溶栓
脑脉通
联合
凋亡
Cerebral ischemia
Rats
Thrombolysis
Naomaitong
Association
Apoptosis
