摘要
目的观察缺血后处理对大鼠急性肾缺血再灌注损伤的抑制作用及其对细胞凋亡的影响。方法建立原位大鼠单侧肾缺血再灌注动物模型，摘除右肾后对左肾行缺血后处理，即10S再灌注，10S缺血，6次循环后再灌注24h。全自动生化分析仪检测血尿素氮（BUN）和肌酐（Cr）含量，比色法测定血浆中脂质过氧化产物丙二醛（MDA）和超氧化物歧化酶（SOD）含量，免疫组织化学法观察肾组织中细胞色素C的表达，流式细胞术检测细胞凋亡率，免疫印迹法（Western blot）检测胞浆中细胞色素C的含量。结果肾缺血再灌注24h后，血中BUN、Cr和MDA明显增高，肾细胞凋亡率明显增加。移植肾经缺血后处理，血中BUN、Cr和MDA含量均降低，SOD含量升高，细胞色素C释放减少，肾细胞凋亡率明显降低。结论缺血后处理可以减轻移植肾脂质过氧化反应，减少’肾细胞凋亡率，减轻肾缺血再灌注损伤。
Objective To investigate the protective effect of ischemic postcondtioning on acute renal ischemia/reperfusion （I/R） injury. Methods A rat I/R model was established. The postconditioning was induced by 6 cycles of reperfusion （10 s） and ischemia （10 s）. The parameters of renal function were determined by auto-biochemical analyzer. The concentrations of malondialdehyde （MDA） and superoxide dismutase （SOD） were measured by chromometry. Cytochrome c （Cyt C） in cytoplasm was examined by immunohistochemistry and Western blot. The renal apoptosis was detected by flow cytometry. Results Compared with the sham group, the release of Cyt C, renal function and MDA were increased significantly in I/R group. After ischemic postconditioning, the levels of BUN, Cr, MDA and apoptosis were significantly decreased and SOD in the serum was significantly increased. Conclusion Ischemic postconditioning can decrease renal I/R injury and inhibit oxidative stress.
出处
《中华器官移植杂志》
CAS
CSCD
北大核心
2008年第2期94-97,共4页
Chinese Journal of Organ Transplantation
基金
国家自然科学基金（30672107）
关键词
缺血再灌注损伤
缺血后处理
细胞凋亡
Ischemia-reperfusion injury
Ischemic postconditioning
Apoptosis
