Ischemic postconditioning inhibits apoptosis after renal ischemia/reperfusion injury in rat

被引:70
作者
Chen, Hui [1 ]
Xing, Bianzhi [2 ]
Liu, Xiuheng [1 ]
Zhan, Bingyan [1 ]
Zhou, Jiangqiao [1 ]
Zhu, Hengcheng [1 ]
Chen, Zhiyuan [1 ]
机构
[1] Wuhan Univ, Renmin Hosp Wuhan Univ, Dept Urol, Wuhan 430060, Peoples R China
[2] HUST, Tongji Med Coll, Tongji Hosp, Dept Neurol, Wuhan, Peoples R China
关键词
apoptosis; ischemia/reperfusion; ischemic postconditioning; kidney;
D O I
10.1111/j.1432-2277.2007.00606.x
中图分类号
R61 [外科手术学];
学科分类号
摘要
Ischemic postconditioning is a phenomenon that intermittent interruptions of blood flow in the early phase of reperfusion can protect organ from ischemia/ reperfusion (I/R) injury. In the present study, we investigated whether the protective effect of ischemic postconditioning was associated with modulation of apoptosis after renal I/R injury. Rats were subjected to 45 min of renal ischemia, both with and without treatment with ischemic postconditioning. Serum urea nitrogen and creatinine levels, phosphorylation of Akt and ERK1/2 and apoptosis were compared after renal injury. Our data showed that ischemic postconditioning attenuated the renal dysfunction and cell apoptosis induced by I/R and increased phosphorylation of Akt and ERK1/2. The results indicated that ischemic postconditioning decreased apoptosis and improved renal function. This protective effect may be related with the levels of Akt and ERK1/2 activation. These findings may have major implications in the treatment of renal transplantation.
引用
收藏
页码:364 / 371
页数:8
相关论文
共 41 条
[1]   Ischemic preconditioning in solid organ transplantation: from experimental to clinics [J].
Ambros, Joan Torras ;
Herrero-Fresneda, Immaculada ;
Borau, Oscar Gulias ;
Boira, Josep M. Grinyo .
TRANSPLANT INTERNATIONAL, 2007, 20 (03) :219-229
[2]   Inhibition of Bax channel-forming activity by Bcl-2 [J].
Antonsson, B ;
Conti, F ;
Ciavatta, A ;
Montessuit, S ;
Lewis, S ;
Martinou, I ;
Bernasconi, L ;
Bernard, A ;
Mermod, JJ ;
Mazzei, G ;
Maundrell, K ;
Gambale, F ;
Sadoul, R ;
Martinou, JC .
SCIENCE, 1997, 277 (5324) :370-372
[3]   Modulation of the mitochondrial permeability transition by nitric oxide [J].
Balakirev, MY ;
Khramtsov, VV ;
Zimmer, G .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 1997, 246 (03) :710-718
[4]   Role of apoptosis in the pathogenesis of acute renal failure [J].
Bonegio, R ;
Lieberthal, W .
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION, 2002, 11 (03) :301-308
[5]   PI3-kinase regulates the mitochondrial transition pore in controlled reperfusion and postconditioning [J].
Bopassa, JC ;
Ferrera, R ;
Gateau-Roesch, O ;
Couture-Lepetit, E ;
Ovize, M .
CARDIOVASCULAR RESEARCH, 2006, 69 (01) :178-185
[6]  
Daemen MARC, 2002, TRANSPLANTATION, V73, P1693
[7]   Inhibition of apoptosis induced by ischemia-reperfusion prevents inflammation [J].
Daemen, MARC ;
van't Veer, C ;
Denecker, G ;
Heemskerk, VH ;
Wolfs, TGAM ;
Clauss, M ;
Vandenabeele, P ;
Buurman, WA .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (05) :541-549
[8]  
Daemen MARC, 2001, TRANSPLANTATION, V71, P1007
[9]   Postconditioning via stuttering reperfusion limits myocardial infarct size in rabbit hearts: role of ERK1/2 [J].
Darling, CE ;
Jiang, R ;
Maynard, M ;
Whittaker, P ;
Vinten-Johansen, J ;
Przyklenk, K .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2005, 289 (04) :H1618-H1626
[10]   Mitochondrial membrane permeabilisation by Bax/Bak [J].
Esposti, MD ;
Dive, C .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2003, 304 (03) :455-461