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目的探讨肾缺血预处理和缺血后处理对肾缺血-再灌注(I-R)损伤的影响机制。方法SD大鼠50只均分为假手术组(A组)、I-R(B组)、缺血预处理组(C组)、缺血后处理组(D组)和联合处理组(E组)。缺血45min再灌注24h后取肾,检测一氧化氮(NO)含量、一氧化氮合酶(NOS)活性、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量;HE染色观察肾组织病理变化情况,并进行中性粒细胞(PMN)计数和Paller′s评分;TUNEL法观察肾组织细胞凋亡情况。结果与B组比较,C、D、E组的SCr、BUN显著降低、肾组织MDA含量显著减少、肾组织SOD活性和肾NOS、NO水平显著增加、肾小管上皮细胞阳性凋亡率显著降低(P<0.01)。结论缺血预处理和缺血后处理均能够减轻肾I-R损伤,可能与其增加NOS在肾脏的表达有关。
Objective To investigate the mechanism of renal ischemic preconditioning and ischemic postconditioning on renal ischemia-reperfusion (I-R) injury. Methods Fifty SD rats were randomly divided into sham operation group (A group), IR group (B group), ischemic preconditioning group (C group), ischemic postconditioning group (D group) and combined treatment group (E group) . The rats were sacrificed at 45 min after ischemia and 24 h after reperfusion. The contents of nitric oxide (NO), nitric oxide synthase (NOS), superoxide dismutase (SOD) and malondialdehyde (MDA) The pathological changes of renal tissue were observed. Neutrophil count (PMN) and Paller’s score were also measured. TUNEL method was used to observe the apoptosis of renal tissue. Results Compared with group B, the levels of SCr and BUN were significantly decreased in group C, D and E, the content of MDA in kidney tissue was significantly decreased, the activity of SOD and the level of NOS and NO in renal tissue were significantly increased, and the apoptosis rate of renal tubular epithelial cells was significantly decreased P <0.01). Conclusion Both ischemic preconditioning and ischemic postconditioning can reduce renal I-R injury, which may be related to the increased expression of NOS in the kidney.