中文摘要：

目的探讨醌型二氢生物喋呤还原酶（ quinoid dihydropteridine reductase, QDPR）表达变化对高糖环境下肾小管上皮细胞系 NRK-52E氧化应激的影响。方法利用慢病毒技术构建过表达及敲低QDPR基因的NRK-52E模型及其对照组,分别给予5.4 mmol/L及30 mmol/L葡萄糖培养基模拟正常及高糖环境,用流式细胞术dihydroethidium法检测各组细胞超氧阴离子（ O-2）含量。 Western印迹法检测超氧化物歧化酶1（superoxide dismutase 1, SOD1）在各组表达水平。结果高糖环境下,过表达QDPR基因组与空载对照组相比细胞O-2含量降低（P〈0.01）,SOD1表达下调（P〈0.01）。低表达QDPR基因组与随机序列对照组相比O-2含量升高（P〈0.05）,SOD1表达无明显变化。结论高糖环境下,QDPR基因高表达能降低NRK-52E细胞氧化应激,沉默QDPR基因能增加NRK-52E细胞氧化应激。 QDPR基因可能通过影响氧化应激而影响糖尿病肾病的发生发展。

英文摘要：

Objective To study whether quinoid dihydropteridine reductase （ QDPR ） expression level change can affect oxidative stress of NRK-52E renal tubular cells in a high glucose environment. Methods The NRK-52E model of overexpression, knockdown QDPR gene and respective control were constructed by lentivirus. All groups were given 5. 4 mmol/L and 30 mmol/L glucose culture medium respectively to imitate normal and high glucose condition. The level of superoxide anion （ O-2 ） was detected by flow cytometer dihydroethidium method. The protein expression level of superoxide dismutase 1 （SOD1）was tested by Western blot. Results QDPR over-expression can decrease O-2（P〈0. 01）and SOD1（P〈0. 05）levels in high glucose condition;QDPR knockdown increases O-2（P〈0. 01） and does not change SOD1. Conclusion Under high glucose condition, overexpression of QDPR gene decreases NRK-52E cell oxidative stress. Knockdown QDPR gene increases NRK-52E cell oxidative stress. QDPR gene may influence the development of diabetic nephropathy by oxidative stress.