摘要
目的:探讨急性脑缺血时大鼠肾脏细胞凋亡的动态变化以及钙超载、氧自由基与肾脏细胞凋亡的关系,了解缺血性脑血管病引起肾脏损伤的机制。方法:随机取36 只Wistar大鼠,将其中的6 只作为对照组,另外30只以30、60、90、120、180 min为时限又分为5个实验组。观察各组肾功能、血及肾组织中丙二醛(MDA)浓度、肾组织细胞内钙含量的动态变化以及肾脏细胞凋亡的情况。结果:(1)血清尿素氮(BUN)以及血清肌酐(Cr)水平随缺血时间延长逐渐升高,至180 min时达高峰,对照组与缺血30 min组相比差异有统计学意义(P<0.05);(2)肾脏细胞凋亡指数明显增加,各实验组与对照组相比差异有统计学意义(P<0.01);(3)血清及肾组织中MDA浓度、肾组织细胞内钙含量随时间延长持续升高,60、90、120、180 min 4个实验组与对照组相比差异有统计学意义(P<0.05或0.01); (3)电镜下肾脏细胞有超微结构的改变。结论:当发生急性脑缺血时,大鼠血清及肾组织MDA的浓度、肾组织细胞内钙含量随时间延长持续增加,可通过激活促细胞凋亡的程序而诱导肾脏细胞凋亡。
Objective: To studay the changes of apoptosis of renal cells in rats during acute ceretral ischemia and relations with Ca 2+ and malondialdehyde(MDA). To observe the action mechanisms of renal damage in ischemia cerebrovacular disease. Methods: 36 Wistar rats were randomly divided into the control groups(n=6) and the ischemia group .The ischemia model of rats (n=30) was divided into 5 groups of 30, 60, 90, 120 and 180 min. The following data was obtained:The level of MDA in plasma and renal tissue and the level of Ca 2+ in renal tissue. At the same time the number of renal cells apoptosis were also recorded. Results:(1)The level of BUN and the level of Cr at 180 min showed a notable discrepancy compared to control group and 30min group (P<0.05);(2)The number of renal apoptosis was higher in experimental groups than in control group (P<0.01);(3)The content of MDA between in plasma and in renal tissue at 60, 90, 120 and 180 min were significantly elevated compared to normal control(P<0.05). The content of Ca 2+ in renal tissue elevated, too;(4)Alterations of renal ultrastructure were seen under election miscroscope. Conclusions:The levels of Ca 2+ in renal tissue and MDA in plasma and in renal tissue elevated progressively, which induced renal cells apoptosis through signal conduction. And the decreasing of renal function was consistented with renal pathological changes.
出处
《新疆医科大学学报》
CAS
2005年第3期221-223,共3页
Journal of Xinjiang Medical University
