Both ischemic and pharmacological preconditioning decrease leukocyte/endothelial cell interactions in donor liver in rats
- VernacularTitle:缺血或药物预处理对大鼠供肝缺血再灌注损伤的抑制作用
- Author:
Gang WU
;
Yongfeng LIU
;
Lei YANG
- Publication Type:Journal Article
- Keywords:
Ischemic preconditioning;
Reperfusion injury;
Heat-shock proteins;
Heme oxygenase
- From:
Chinese Journal of Organ Transplantation
2003;0(06):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the molecular mechanisms of delayed ischemic preconditioning (IPC) and doxorubicin preconditioning (DPC) to induce ischemic tolerance. Methods The models of sham-operation and orthotopic liver transplantation in the Wistar rats was used. IPC was administered with a 10-min ischemia followed by a 10-min reperfusion. Animals in the DPC group were pretreatd with Doxorubicin (1?mg/kg, iv). The control rats were subjected to saline treatment. The induction of HSP70 and HO-1 protein ( Western blot), the expression of ICAM-1 transcripts (RT-PCR)and ICAM-1 protein (immunohistochemistry), the activities of serum AST, ALT, LDH, and liver myeloperoxidase (MPO) , liver wet-to-dry weight ratios (W/D) were assessed.Results HO-1 expression was maximally induced at 12?h after IPC, and hardly changed until 48?h. A strong induction of HSP70 was detected at about 24 to 72?h after IPC. The levels of HO-1 and HSP70 were obviously elevated at 24?h after IPC or DPC as compared with the control ( P 0.05 ). In the control group, the transcription of ICAM-1 was significantly increased 6?h after reperfusion. Capillary endothelial cells of the livers strongly expressed ICAM-1. Activities of liver MPO were obviously elevated. IPC and DPC could significantly decrease the transcription of ICAM-1 in the livers in concurrence with the expression of ICAM-1 protein as well as the activity of MPO at 6?h after reperfusion ( P
