摘要
目的研究地佐辛预处理对全脑缺血再灌注大鼠神经元凋亡的作用及其机制。方法将48只健康成年雄性Wistar大鼠随机分为假手术组(S组)、缺血再灌注组(IR组)和地佐辛预处理组(D组)。再灌注24h后取脑组织,采用苏木精-伊红染色观察神经元形态学变化,Western-blot方法测定Caspase-3表达,水溶性四氮唑法测定超氧化物歧化酶(SOD)活性,TUNEL法检测凋亡细胞阳性率。结果与S组比较,其余组凋亡细胞阳性率和Caspase-3表达水平升高,SOD活性下降;与IR组比较,D组凋亡细胞阳性率和Caspase-3表达水平降低,SOD活性升高。差异均有统计学意义(F=4.83~10.66,P<0.05)。结论地佐辛预处理对大鼠脑缺血再灌注神经元有保护作用,且其作用机制与抑制Caspase-3生成和减少氧化应激相关。
Objective To investigate the effect of dezocine preconditioning on neuronal apoptosis in rats with global cerebral ischemia-reperfusion and related mechanisms. Methods A total of 48 healthy male Wistar rats were randomly divided into sham-operation group(S group),ischemia-reperfusion group(IR group),and dezocine preconditioning group(D group).Brain tissue was collected at 24 hafter reperfusion.Hematoxylin and eosin staining was used to observe the morphological changes of neurons;Western-blot was used to measure the expression of caspase-3;water-soluble tetrazolium salt was used to measure the activity of superoxide dismutase(SOD);terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling was used to measure the positive rate of apoptotic neurons. Results Compared with the S group,the IR group and the D group had significant increases in the positive rate of apoptotic neurons and the expression of caspase-3 and a significant reduction in the activity of SOD;compared with the IR group,the D group had significant reductions in the positive rate of apoptotic neurons and the expression of caspase-3 and a significant increase in the activity of SOD(F=4.83-10.66,P〈0.05). Conclusion Dezocine preconditioning can protect the neurons against cerebral ischemia/reperfusion in rats,possibly by inhibiting the expression of caspase-3 and reducing oxidative stress.
作者
毕紫鹏
董河
王立翠
冯伟
贾彦芳
衣选龙
BI Zipeng;DONG He;WANG Licui;FENG Wei;JIA Yanfang;YI Xuanlong(Department of Anesthe siology, The Affiliated Hospital of Qingdao University, Qingdao 266071, China)
出处
《青岛大学学报(医学版)》
CAS
2018年第3期351-353,358,共4页
Journal of Qingdao University(Medical Sciences)
基金
山东省医药卫生科技发展计划项目(2016WS0261)