探讨慢性肾衰竭的大鼠肾脏UCP2的表达变化与肾脏氧化应激水平变化的关系

Relationship between Changes of the Expression of UCP2 and Oxidative Stress in the Kidneys of Rats with Chronic Renal Failure

摘要: 目的：观察慢性肾衰竭大鼠肾脏氧化应激水平的变化与肾脏UCP2表达的变化，探讨二者的相关性。方法：60只雄性SD大鼠随机分为假手术组(sham)和肾衰组(NX)，肾衰组行5/6肾大部切除术，假手术组仅行肾包膜剥离术。分别在第4、8、12周时处死大鼠死，留取血液及肾组织，采用ELISA方法检测血清生化指标肌酐(SCr)及尿素氮(BUN)，肾组织匀浆中超氧化物气化酶(SOD)、谷胱甘肽过氧化物酶(GSH-px)及丙二醛(MDA)，通过Western-blot方法检测肾组织UCP2的表达水平。结果：① 第4、8、12周时，肾衰组大鼠SCr及BUN、水平均显著高于假手术组(P < 0.05)。② 第4、8、12周时，肾衰组大鼠肾组织匀浆中SOD及GSH-px低于假手术组，MDA高于假手术组(P < 0.05)。比较肾衰组，第4和12周时SOD及GSH-px高于第8周、MDA低于第8周(P < 0.05)。③ 第4周时，两组大鼠肾脏UCP2的表达差异无统计学意义(P > 0.05)，第8、12周时，肾衰组UCP2的表达水平高于假手术组(P < 0.05)，12周时最显著(P < 0.05)。结论：随着病程的进展，慢性肾衰竭大鼠肾脏氧化应激状态愈加严重，肾脏UCP2表达的增加可能是应对氧化应激的一种代偿机制，同时减弱氧化应激状态，在慢性肾衰竭发生过程中起到保护作用。

Abstract: Objective: To observe the changes of renal oxidative stress level and the expression of UCP2 in the kidney of rats with chronic renal failure, and to explore the potential correlation between them. Methods: Sixty male SD rats were randomly divided into sham operation group (sham) and chronic renal failure group (NX). Chronic renal failure group underwent 5/6 partial nephrectomy while the sham group only underwent renal capsule dissection. At the 4th, 8th and 12th week, rats were sacrificed to sample blood and kidney tissue. Serum Cr (Scr) and BUN, SOD, GSH-px and MDA levels in kidney were detected by using ELISA. The expression of UCP2 in renal tissues was detected by using Western-blotting. Results: 1) At the 4th, 8th, and 12th week, the levels of SCr and BUN in the chronic renal failure groups were significantly higher than that in the sham groups (P < 0.05). 2) At the 4th, 8th and 12th week, the SOD and GSH-px in the renal tissue homogenate of the rats with renal failure were lower than that of the sham operation groups, and the MDA was higher than that of the sham operation groups (P < 0.05). Compared with the renal failure groups, at 4th and 12th week, SOD and GSH-px were higher than at 8th week, and MDA was lower than 8th week (P < 0.05). 3) At the 4th week, there was no significant difference in the expression of UCP2 in the kidney between the two groups (P > 0.05). At the 8th and 12th week, the expression of UCP2 in the renal failure groups was higher than that in the sham operation groups (P < 0.05). The difference was the most significant at the 12th week. Conclusion: With the progress of the disease, the oxidative stress in the kidney of rats with chronic renal failure is more serious. The increase of renal UCP2 expression may be a compensatory mechanism for oxidative stress, and at meanwhile the lower level of oxidative stress plays a protective role in the development of chronic renal failure.