Hong Li, Wu Jiang, Cai Wei
Department of Pediatric Surgery, Xinhua Hospital and Shanghai Children's Medical Center, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
JPEN J Parenter Enteral Nutr. 2007 May-Jun;31(3):199-204. doi: 10.1177/0148607107031003199.
This study was designed to explore the mechanisms in parenteral nutrition (PN)-associated hepatic dysfunction, and the possible effectiveness of glutathione (GSH) to alleviate this injury.
Thirty 1-week-old New Zealand rabbits were divided into 3 groups: 10 in the control group (maternal fed); 10 in the PN group (PN for 10 days); and 10 in the GSH + PN group (PN plus glutathione for 10 days). At the end of the study, blood biochemistry analysis and liver histologic examination were performed by light and electronic microscope; malondialdehyde (MDA) content of liver tissues and apoptotic hepatocytes were also measured.
Direct bilirubin and bile acid in the PN group were significantly higher than that in the control group and in the GSH + PN group (p < .05, for both). In the PN group, there were some cholestatic or steatotic changes. In the GSH + PN group, histologic changes were reduced compared with the PN group. The electron microscopy appearances were in agreement with the histologic findings. MDA value was higher in the PN group than in the control group and in the GSH + PN group (p < .05, respectively). Terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL) assays showed that the rate of apoptotic hepatocytes in the PN group was the highest and the control group was the lowest among 3 groups (comparison between groups, p < .01, individually.)
The study showed that PN can induce hepatic dysfunction in infant rabbits. GSH can effectively reduce this injury. The study implies that oxidative stress and apoptosis contribute to PN-associated hepatic dysfunction.
本研究旨在探讨肠外营养（PN）相关肝损伤的机制，以及谷胱甘肽（GSH）减轻该损伤的可能效果。
将30只1周龄新西兰兔分为3组：对照组10只（母兔喂养）；PN组10只（接受PN 10天）；GSH + PN组10只（接受PN加谷胱甘肽10天）。研究结束时，进行血液生化分析及肝脏组织学检查（光镜和电镜）；同时测定肝组织丙二醛（MDA）含量及凋亡肝细胞数量。
PN组直接胆红素和胆汁酸显著高于对照组及GSH + PN组（均p < 0.05）。PN组出现一些胆汁淤积或脂肪变性改变。与PN组相比，GSH + PN组组织学改变减轻。电镜表现与组织学结果一致。PN组MDA值高于对照组及GSH + PN组（分别p < 0.05）。末端脱氧核苷酸转移酶介导的缺口末端标记（TUNEL）检测显示，PN组凋亡肝细胞率最高，对照组最低（组间比较，均p < 0.01）。
本研究表明PN可诱导幼兔肝损伤。GSH可有效减轻该损伤。本研究提示氧化应激和细胞凋亡与PN相关肝损伤有关。
