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机构地区:[1]广东省深圳市第五人民医院急诊科,广东深圳518001
出 处:《吉林医学》2013年第23期4643-4644,共2页Jilin Medical Journal
摘 要:目的:研究热休克应答对大鼠脑缺血再灌注后神经细胞凋亡的影响,探索热休克蛋白70治疗缺血性再灌注损伤的应用前景。方法:将46只成年Wistar大鼠随机分为假手术组、对照组与试验组。除假手术组大鼠外,其余大鼠均制作全脑缺血再灌注动物模型,对照组不进行热休克应答干预,试验组在全脑缺血再灌注后进行热休克干预,即静脉注射热休克蛋白70,分别于不同时间段(6小时、12小时)检测各组大鼠脑神经细胞凋亡数目,对比分析各组大鼠神经细胞凋亡情况的差异,验证热休克蛋白70对大鼠脑缺血再灌注后神经细胞凋亡的保护作用。结果:与对照组比较,试验组大鼠脑神经细胞凋亡数目减少,差异有统计学意义(P<0.05)。结论:热休克应答对大鼠脑缺血再灌注后神经细胞凋亡有保护性作用,热休克蛋白70对缺血性脑血管病再灌注损伤有一定的治疗前景。Objective To investigate the effect of Heat shock reaction on neuronal apoptosis after inchemina reperfusion injury in rats. To explore the feasible prospect of heat shock protein 70 on ischemic cerebral vascular disease. Methods 46 Wistar rats were randomly di- ~ded into the sham operation group.the control group and the treatment group. The sham operation group received neither BCCO model made nor further treatment,the control group received BCCO model made but not HSP70 injection and the treatment group received both. The count of neuronal apoptosis was measured respectively at 6h .12h ater injection heat shock protein 70. To contrast the differences of neuronal apoptosis among groups in order to verify the protective effect of HSP'/0 on neuronal apoptisis after inchemina reperfusion ingury in rata. Results To comprare with the control group, the counts of neuronal apoptosis were reduced in rats of treatment group. The difference was statistically significant. Conclusion Heat shock reaction has the effect of preventing neronal cell from apoptosis after inchemina r^perfu- slon injury in rats and heat shock protein 70 has the feasible prospect on ischemic ecrebralvascular disease.
分 类 号:R743[医药卫生—神经病学与精神病学]
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