摘要
目的研究缺血后处理减轻大鼠肾脏缺血-再灌注损伤的细胞凋亡的作用.方法大鼠右肾切除,左肾45min缺血再灌注6h,给予6个循环10s/10s再灌/停灌缺血后处理方案干预后,测定血肌酐和尿素氮水平评价肾功能;HE染色观察肾组织病理形态学变化;原位末端脱氧核苷酸转移酶标记(TUNEL)法检测肾组织中凋亡细胞,;Western blotting法检测肾组织Bcl-2和Bax蛋白表达.结果缺血后处理能明显减轻肾组织病理形态学损伤,降低血肌酐和尿素氮水平(P<0.05),减轻缺血-再灌注损伤后的细胞凋亡(P<0.05),增加Bcl-2的表达和降低Bax的表达(P<0.05).结论缺血后处理可减轻肾脏缺血-再灌注损伤,其保护作用可能与上调Bcl-2蛋白和下调Bax蛋白从而抑制再灌注损伤的细胞凋亡有关.
Objictive To investigate the protective effect of ischemic postconditioning（IPostC） against apoptosis after renal ischemic reperfusion injury.Methods After right nephrectomy,rats were subjected to 45 min of left renal ischemia followed by 6 h reperfusion.IPostC was conducted by six cycles of 10 sec reperfusion/10 sec renal pedicle occlusion at the end of ischemia,followed by 6 h reperfusion.Renal function was evaluated by detecting the levels of serum creatine and urea nitrogen;the renal pathologic change was observed by HE staining;apoptosis was detected by TUNEL method;Western blotting was used to evaluate the protein expression of Bcl-2and Bax.Results Our data showed that ischemic postconditioning decreased the levels of serum creatine and urea nitrogen,and improved the renal pathologic change.Ischemic postconditioning attenuated cell apoptosis induced by ischemic reperfusion（P 0.05） ,increased the protein expression of Bcl-2 and decreased the protein expression of Bax（P 0.05） .Conclusions Ischemic postconditioning can improve renal function and inhibit cell apoptosis.The protective effect may be related with the upregulation of the protein expression of Bcl-2 and the downregulation of the protein expression of Bax.
出处
《昆明医学院学报》
2010年第5期17-23,共7页
Journal of Kunming Medical College
基金
昆明医学院研究生创新基金资助项目(11415018)
关键词
缺血-再灌注损伤
缺血后处理
缺血预处理
细胞凋亡
肾脏
Ischemic reperfusion injury
Ischemic postconditoning
Ischemic preconditioning
Apoptosis
Kidney
