Mitochondria-initiated apoptosis triggered by oxidative injury play a role in total parenteral nutrition-associated liver dysfunction in infant rabbit model
Mitochondria-initiated apoptosis triggered by oxidative injury play a role in total parenteral nutrition-associated liver dysfunction in infant rabbit model
复制标题
氧化损伤引发的线粒体引发的细胞凋亡在幼兔模型全肠外营养相关肝功能障碍中发挥作用
DOI：
10.1016/j.jpedsurg.2009.04.002
复制
发表时间：
2009-09-01
影响因子：
2.4
通讯作者：
Cai, Wei
中科院分区：
文献类型：
--
作者：
Hong, Li;Wang, Xiang;Cai, Wei
目的：本研究的目的是探讨氧化损伤和细胞凋亡作为机制的基础全胃肠外营养（TPN）相关的肝功能fundamental.Methods：20新西兰兔（2周龄）分为2组，如下：10个对照组（母体饲料）和10个在TPN组。结果：TPN组家兔经右颈静脉置管持续输注PN 10 d后，TPN组家兔血清总胆红素和胆汁酸水平明显高于对照组（P <0.01）;光镜下可见炎性细胞浸润和脂肪变性。电子显微镜下可见胞浆空泡和微胆管内少见的微绒毛改变。此外，10天的治疗导致肝细胞超氧化物歧化酶（SOD）活性的抑制，丙二醛水平的增加，细胞色素c从线粒体释放的显着增加，caspase 3活性显着增加，并增加细胞凋亡（P <0.01，单独）。结论：氧化损伤可能是TPN相关的肝功能障碍的重要机制之一。此外，氧化损伤引发的细胞凋亡可能在这一过程中发挥重要作用。(c)2009 Elsevier Inc. All rights reserved.
Purpose: The aim of the study was to investigate oxidative injury and apoptosis as the mechanisms underlying total parenteral nutrition (TPN)-associated liver dysfunction.Methods: Twenty New Zealand rabbits (2 weeks old) were divided into 2 groups as follows: 10 in the control group (maternal feed) and 10 in the TPN group. The rabbits in the TPN group received continuous PN infusion through a silastic catheter inserted in the right jugular vein.Results: After 10 days of treatment, the scrum levels of total bilirubin and bile acid were significantly higher in the TPN group than in the control group (P < .01, respectively). The light microscopic findings in the TPN rabbits included inflammatory cell infiltration and hepatic steatosis. Electron microscopy showed change in the cytosolic vacuoles and rare microvilli in the microbile duct. Moreover, 10 days of treatment resulted in an inhibition of the superoxide dismutase (SOD) activity in hepatocytes, an increase of the malondialdehyde level, a significant increase in cytochrome c release from the mitochondria, a significant increase in caspase 3 activity, and increased apoptosis (P < .01, individually).Conclusions: Oxidative damage may be one of the essential mechanisms of TPN-associated liver dysfunction. Moreover, mitochondria-initiated apoptosis triggered by oxidative damage may play an important role in this process. (c) 2009 Elsevier Inc. All rights reserved.