Burne M J, Haq M, Matsuse H, Mohapatra S, Rabb H
Division of Nephrology, Hennepin County Medical Center, University of Minnesota, Minneapolis 55415, USA.
Transplantation. 2000 Mar 15;69(5):1023-5. doi: 10.1097/00007890-200003150-00065.
The development of genetically engineered mice has led to increased use of mouse models to study renal ischemic reperfusion injury (IRI). We hypothesized that susceptibility to IRI could result from strain differences due to genetic factors.
Our study compared recovery subsequent to renal IRI in NIH Swiss, C57BL/6, and BALB/c mice. Serum creatinine (SCr) and blood urea nitrogen (BUN) levels were evaluated postischemia. We also conducted reverse transcriptase-polymerase chain reaction (RT-PCR) analyses of renal cytokines and adhesion molecules postischemia.
At 48 hr postischemia, renal dysfunction in NIH Swiss mice was significantly reduced, compared with other groups (P<0.01). BUN measurements confirmed renal protection at 48 hr in the NIH Swiss group. RT-PCR analysis of mRNA postischemia demonstrated that, between strains, there was little difference in mRNA expression for renal cytokines and adhesion molecules.
NIH Swiss mice appear to be resistant in susceptibility to renal IRI. Early expression of pro-inflammatory genes was not associated with resistance to IRI, thus genetic factors could be important in outcome after renal IRI.
基因工程小鼠的发展使得小鼠模型在研究肾缺血再灌注损伤（IRI）中的应用增加。我们推测，IRI易感性可能源于遗传因素导致的品系差异。
我们的研究比较了NIH瑞士小鼠、C57BL/6小鼠和BALB/c小鼠肾IRI后的恢复情况。缺血后评估血清肌酐（SCr）和血尿素氮（BUN）水平。我们还在缺血后对肾细胞因子和黏附分子进行了逆转录聚合酶链反应（RT-PCR）分析。
缺血后48小时，与其他组相比，NIH瑞士小鼠的肾功能障碍明显减轻（P<0.01）。BUN测量结果证实NIH瑞士组在48小时时有肾脏保护作用。缺血后mRNA的RT-PCR分析表明，各品系之间肾细胞因子和黏附分子的mRNA表达差异不大。
NIH瑞士小鼠似乎对肾IRI易感性具有抗性。促炎基因的早期表达与对IRI的抗性无关，因此遗传因素可能在肾IRI后的结果中起重要作用。
