Cavalieri Barbara, Perrelli Maria-Giulia, Aragno Manuela, Mastrocola Raffaella, Corvetti Giovanna, Durazzo Marilena, Poli Giuseppe, Cutrìn Juan C
Laboratory of Experimental Liver Pathology, the Department of Clinical and Biological Sciences, University of Turin, Italy.
Liver Transpl. 2002 Nov;8(11):990-9. doi: 10.1053/jlts.2002.35549.
In an in vivo rat model of liver ischemia followed by reperfusion a consistent appearance of necrosis and activation of biochemical pathways of apoptosis was reproduced and monitored after 30 minutes reperfusion. Preconditioning by application of a short cycle of ischemia-reperfusion (10 minutes + 10 minutes) positively conditioned recovery of the organ at reperfusion, attenuating both necrotic and apoptotic events. Preconditioning at least halved cell oxidative damage occurring early at reperfusion, and as a major consequence, the increase of cytolysis and apoptosis occurring at reperfusion was about 50% less. The attenuation of both pathways of cell death by preconditioning appeared at least partly related to its modulate action on H(2)O(2) and 4-hydroxy-2,3-trans-nonenal production. The overall data point to a marked diminished oxidant generation and oxidative reactions as one major possible mechanism through which ischemic preconditioning exerts protection against necrotic and apoptotic insult to the postischemic liver.
在大鼠肝脏缺血再灌注的体内模型中，再灌注30分钟后再现并监测到坏死的一致表现以及凋亡生化途径的激活。通过应用短周期的缺血再灌注（10分钟 + 10分钟）进行预处理，可使器官在再灌注时得到积极的恢复条件，减轻坏死和凋亡事件。预处理至少将再灌注早期发生的细胞氧化损伤减半，并且作为主要结果，再灌注时发生的细胞溶解和凋亡增加减少了约50%。预处理对细胞死亡两条途径的减轻作用似乎至少部分与其对过氧化氢和4-羟基-2,3-反式壬烯醛生成的调节作用有关。总体数据表明，氧化产物生成和氧化反应显著减少是缺血预处理对缺血后肝脏坏死和凋亡损伤发挥保护作用的一种主要可能机制。
