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Both ischemic and pharmacological preconditioning decrease leukocyte/endothelial cell interactions in donor liver in rats
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- Author:
- No author available
- Journal Title:
- CHINESE JOURNAL OF ORGAN TRANSPLANTATION
- Issue:
- 6
- DOI:
- 10.3760/cma.j.issn.0254-1785.2003.06.106
- Key Word:
- 缺血预处理;再灌注损伤;热休克蛋白70;血红素氧化酶
Abstract： 目的探讨缺血预处理(IPC)或阿霉素预处理(DPC,模拟IPC)对大鼠供肝延迟性保护作用的发生机制.方法将供鼠分为3组. IPC组:供鼠采用肝脏预先缺血10min后再开放;DPC组:供鼠经静脉注射阿霉素(1mg/kg体重);对照组:供鼠用等量生理盐水注射.观察各组预处理后血红素氧化酶-1(HO-1)和热休克蛋白70(HSP70)含量;建立上述各组大鼠原位肝移植模型,并设假手术对照组,观察肝移植后各组对供肝缺血再灌注损伤的影响.结果 IPC组HO-1、HSP70含量分别于预处理12h和24h达到高峰;IPC和DPC组预处理24h,诱导的HSP70、HO-1含量差异无显著性(P>0.05).对照组肝移植后6h,肝组织中ICAM-1 mRNA表达和内皮细胞ICAM-1分子表达明显增强,髓过氧化物酶(MPO)活性增高,血清中天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)、乳酸脱氢酶(LDH)及肝组织湿重/干重(W/D)水平明显升高,和假手术组相比,差异有显著性(P<0.01).IPC或DPC组肝移植后减弱了ICAM-1 mRNA和蛋白表达及MPO活性, AST、ALT、LDH及W/D的水平亦明显降低,与对照组比较,差异有显著性(P<0.05).结论 IPC的延迟保护作用是通过降低中性粒细胞的粘附浸润来实现的,这与IPC 诱导生成HSP70和HO-1有关.DPC可以模拟IPC的延迟性保护作用.
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