摘要
目的研究大鼠肾脏内质网应激(endoplasmic reticulum stress,ERS)与急性缺血性肾损伤(acute kidney injury,AKI)的关系。方法30只雄性SD大鼠采用随机数字表法分为假手术组(n=6)和模型组(n=24),模型组下设缺血40 min再灌注1、6、12、24 h 4个时相点,每个时相点6只。采用自动生化分析仪检测大鼠血肌酐、尿素氮水平。采用PAS染色检测肾小管损伤情况,免疫组化技术检测肾组织ERS标志物GRP78蛋白表达。结果①血肌酐在缺血再灌注(ischemic/reperfusion,I/R)后1 h明显升高,12 h达高峰,24 h下降(P<0.05)。肾小管损伤评分在I/R后1 h升高,12 h达高峰,24 h下降(P<0.05)。②肾组织中GRP78蛋白表达在I/R后6 h升高达高峰,至12 h仍持续较高水平(P<0.05),24 h时下降。③GRP78表达与肾小管损伤呈显著正相关性(r=0.671,P<0.05),也与血肌酐水平呈显著正相关性(r=0.559,P<0.05)。结论肾I/R启动了ERS,并且ERS与肾小管损伤、血肌酐水平呈正相关关系。ERS可能在AKI中起重要作用。
Objective To observe the relationship between endoplasmic reticulum stress and ischemia acute renal injury. Methods The renal ischemia and repeffusion model was developed by bilateral clamping of the renal pedicle for 40 rain and repeffusing for 1, 6,12 and 24 h, respectively. Blood SCr and BUN were detected. Renal tubular injury was measured by PAS staining. The expression of ERS marker , GRP78 protein, in the isehemic renal tissue was detected by immunohistochemistry. Results Scr increased initially at I/R 1 h, reaching a peak at I/R 12 h, and decayed at I/R 24 h . The score of renal tubular injury increased at I/R 1 h, reaching a peak at I/R 12 h, and decayed at I/R 24 h. The expression of GRP78 protein reached the peak at I/R 6 h, maintaining a high level at I/R 12 h, and declined at I/R 24 h. The expression of GRP78 protein had positive correlation with renal tubular injury, and Scr. Conclusion ERS is started after renal I/R in rats. It may play an important role in AKI.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2009年第11期1002-1004,共3页
Journal of Third Military Medical University
基金
国家自然科学基金(30771002)~~
关键词
内质网应激
GRP78
肾缺血再灌注
endoplasmie reticulum stress
GRP78
renal ischemia/repeffusion
作者简介
姚凤华，女，湖北省红安县人，硕士研究生，主治医师，主要从事肾脏病基础方面的研究．E—mail：yaofenghuahh@yahoo.com.cn
通信作者：何娅妮，电话：（023）68757871
