Ischemic preconditioning reduces caspase-related intestinal apoptosis

被引:23
作者
Aban, N
Cinel, L
Tamer, L
Aktas, A
Aban, M
机构
[1] Mersin SSK Hosp, Dept Surg, Mersin, Turkey
[2] Mersin Univ Sch Med, Dept Pathol, Mersin, Turkey
[3] Mersin Univ Sch Med, Dept Biochem, Mersin, Turkey
[4] Mersin Univ Sch Med, Dept Obstet & Gynecol, Mersin, Turkey
关键词
ischemia reperfusion; ischemic preconditioning; apoptosis; caspase; intestine;
D O I
10.1007/s00595-004-2918-y
中图分类号
R61 [外科手术学];
学科分类号
摘要
Purpose. To investigate the preventive effect of ischemic preconditioning (IPC) on ischemia/reperfusion (I/R)-induced apoptosis and injury in the rat intestine. Methods. We divided 30 male Wistar rats, weighing 300-350g, randomly into three groups. The control group rats (n=10) were subjected to laparotomy only; the I/R group (n=10) rats were subjected to occlusion of the superior mesenteric artery for 45 min, followed by reperfusion for 60 min; and the IPC group (n=10) rats were subjected to IPC, achieved with two cycles of 5 min ischemia and 5 min reperfusion immediately before the I/R, as in the I/R group. Blood samples were collected by cardiac puncture, to measure nitrate and myeloperoxidase (MPO) levels. Histopathological and immunohistochemical studies were done to evaluate the I/R-induced apoptosis and injury. Results. The blood MPO and nitrate levels were increased in the I/R group, but IPC prevented their increase. There were significantly fewer apoptotic cells in the IPC group than in the I/R group, and this finding was supported by the caspase-3 expression in the ileum. The intestinal histopathology was also protected by IPC against I/R-induced injury. Conclusion. Ischemic preconditioning clearly prevented I/R-induced injury and apoptosis by a mechanism related to the caspase-3-dependent pathway. We also showed that IPC inhibited leukocyte activation, with the suppression of myeloperoxidase levels in I/R and nitric oxide-related oxidoinflammatory pathway upregulation.
引用
收藏
页码:228 / 234
页数:7
相关论文
共 40 条
[1]  
Aksöyek S, 2002, SHOCK, V18, P476
[2]  
[Anonymous], METHODS ENZYMOLOGY
[3]  
Beckman JS, 1996, AM J PHYSIOL-CELL PH, V271, pC1424
[4]   OXIDATIVE STRESS AS A MEDIATOR OF APOPTOSIS [J].
BUTTKE, TM ;
SANDSTROM, PA .
IMMUNOLOGY TODAY, 1994, 15 (01) :7-10
[5]  
Carden DL, 2000, J PATHOL, V190, P255, DOI 10.1002/(SICI)1096-9896(200002)190:3<255::AID-PATH526>3.0.CO
[6]  
2-6
[7]  
CHIU CJ, 1970, ARCH SURG-CHICAGO, V101, P478
[8]   Ischemic preconditioning reduces intestinal epithelial apoptosis in rats [J].
Cinel, I ;
Avlan, D ;
Cinel, L ;
Polat, G ;
Atici, S ;
Mavioglu, I ;
Serinol, H ;
Aksoyek, S ;
Oral, U .
SHOCK, 2003, 19 (06) :588-592
[9]   Nitric oxide synthase, poly (ADP-ribose) synthetase, and ischemic preconditioning [J].
Cinel, I ;
Oral, U .
CRITICAL CARE MEDICINE, 2002, 30 (09) :2167-2168
[10]   Persistent inhibition of cell respiration by nitric oxide:: Crucial role of S-nitrosylation of mitochondrial complex I and protective action of glutathione [J].
Clementi, E ;
Brown, GC ;
Feelisch, M ;
Moncada, S .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (13) :7631-7636