摘要
目的观察miRNA-92a在缺血再灌注(I/R)损伤4h、24h后小鼠肾组织的表达变化,探讨肾脏缺血损伤后血管生成的可能机制。方法采用双侧夹闭小鼠肾蒂的方法制备急性缺血再灌注肾损伤模型,术后灌注24h后收集血清和肾脏标本,分别检测肾功能及观察肾组织病理学改变。实时定量逆转录聚合酶链反应(real-time RT-PCR)的方法检测小鼠I/R损伤4h和24h组中miRNA-92a的表达水平。结果(1)采用血清肌酐(Scr)和尿素氮(UN)评估肾功能,肾脏I/R24h组与假手术组(sham)比较有显著性差异(P<0.05);HE染色观察肾组织病理改变明显,肾缺血再灌注模型成功。(2)而I/R4h和24h后,miRNA-92a的表达上调,其上调倍数分别为3.23±0.74,1.53±0.33(P<0.05)。结论小鼠I/R损伤中miRNA-92a表达显著上调,miRNA-92a可能参与缺血再灌注肾组织损伤的血管再生的调控过程。
Objective To investigate the expression change of miRNA-92a in kidney ischemia/repeffusion （I/R） injury in mice. Methods Mice were subjected to a standard renal I/R to induce acute kidney injury （AKI） after 45 min of bilateral renal artery clamping, miRNA-92a expression changes used quantitative RT-PCR analysis at 4h and 24h. Results （1）Blood samples were obtained at 24 h and at the time of animal death to evaluate the degree of AKI according to serum creatinine （SCr） and urea nitrogen（UN）（P〈0.05）, and the renal tissues were obtained to evaluate histological changes after I/R at 24h. （2） Quantitative RT-PCR analysis showed that ischemic kidney injury significantly increased miRNA-92a expression compared to the sham controls, with prominent changes at 4h and 24h after reperfusion （n=3each, P〈0.05）. Conclusions Renal I/R to induce AKI significantly increased miRNA-92a expression compared to the sham-operated controls, with prominent changes at 4h and 24h after reperfusion. These results provided evidence that miRNA-92a may be involve the mechanisms of ischemic injury disease and controlled angiogenesis.
出处
《实验与检验医学》
CAS
2010年第1期9-11,共3页
Experimental and Laboratory Medicine
基金
国家自然科学基金(30960385)
