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首页> 外文期刊>American Journal of Physiology >Poly(ADP-ribose) polymerase triggers the microvascular mechanisms of hepatic ischemia-reperfusion injury.
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Poly(ADP-ribose) polymerase triggers the microvascular mechanisms of hepatic ischemia-reperfusion injury.

机译：聚（ADP-核糖）聚合酶触发肝缺血再灌注损伤的微血管机制。

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摘要

Activation of poly(ADP-ribose) polymerase (PARP) mediates oxidative stress-induced cell injury. We tested the hypothesis that PARP contributes to ischemia-reperfusion (I/R) damage of the liver by triggering the mechanisms of microcirculatory failure. Leukocyte- and platelet-endothelial cell interactions as well as sinusoidal perfusion were analyzed by intravital fluorescence microscopy after lobar hepatic I/R (90 min/30 min) in C57BL/6 x 129/Sv wild-type (PARP+/+) and PARP-deficient (PARP-/-) mice. Hepatic I/R induced leukocyte/platelet-endothelial cell interactions and tissue injury in PARP+/+ mice, as indicated by impaired sinusoidal perfusion and increased alanine aminotransferase (ALT)/aspartate aminotransferase (AST) serum activities. In PARP-/- mice, however, the postischemic increase in the numbers of rolling/adherent leukocytes and platelets was significantly lower. In addition, I/R-induced translocation of CD62P as well as mRNA expression of CD62E, CD54, and CD106 were attenuated. The degree of perfusion failure was reduced and the increase in the ALT/AST activities was lower in PARP-/- mice compared with PARP+/+ mice. We conclude that PARP contributes to hepatic microvascular injury by triggering the expression/translocation of adhesion molecules and modulating leukocyte/platelet-endothelial cell interactions.
机译：聚（ADP-核糖）聚合酶（PARP）的激活介导氧化应激诱导的细胞损伤。我们测试了以下假设：PARP通过触发微循环衰竭机制促进肝脏缺血再灌注（I / R）损伤。在C57BL / 6 x 129 / Sv野生型（PARP + / +）和PARP中，肝I / R（90分钟/ 30分钟）后，通过活体荧光显微镜分析白细胞和血小板-内皮细胞的相互作用以及正弦曲线灌注缺陷（PARP-/-）小鼠。肝I / R诱导PARP + / +小鼠中的白细胞/血小板-内皮细胞相互作用和组织损伤，如正弦曲线灌注受损和丙氨酸氨基转移酶（ALT）/天冬氨酸氨基转移酶（AST）血清活性增加所表明。然而，在PARP-/-小鼠中，缺血/后滚动/粘附白细胞和血小板数量的增加明显降低。此外，I / R诱导的CD62P易位以及CD62E，CD54和CD106的mRNA表达减弱。与PARP + / +小鼠相比，PARP-/-小鼠的灌注衰竭程度降低了，ALT / AST活性的增加也降低了。我们得出结论，PARP通过触发粘附分子的表达/转运和调节白细胞/血小板-内皮细胞相互作用来促进肝微血管损伤。

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