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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 486148, 10 pages
Research Article

Glutathione Supplementation Attenuates Oxidative Stress and Improves Vascular Hyporesponsiveness in Experimental Obstructive Jaundice

1Department of Anesthesia & Intensive Care, Eastern Hepatobiliary Surgery Hospital, the Second Military Medical University, Shanghai 200438, China
2Department of Anesthesiology, 81st Hospital of the Chinese PLA, Nanjing 210002, China

Received 24 September 2014; Revised 31 January 2015; Accepted 31 January 2015

Academic Editor: Yanfang Chen

Copyright © 2015 Jiaying Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


We investigated the protective effects and mechanism of glutathione (GSH) on vascular hyporesponsiveness induced by bile duct ligation (BDL) in a rat model. Seventy-two male Sprague-Dawley rats were randomly divided into four groups: a NS group, a GSH group, a BDL + NS group, and a BDL + GSH group. GSH was administrated into rats in the GSH and BDL + GSH groups by gastric gavage. An equal volume of normal saline was, respectively, given in the NS group and BDL + NS group. Blood was gathered for serological determination and thoracic aorta rings were isolated for measurement of isometric tension. Obstructive jaundice led to a significant increase in the serum total bilirubin, AST, and ALT levels. The proinflammatory cytokines levels (TNF-α and IL-1β), concentration of NO, and oxidative stress markers (MDA and 3-NT) were increased as well. All of those were reduced by the treatment of GSH. Meanwhile, contraction of aorta rings to NA and vasorelaxation to ACh or SNP in the BDL group rats were markedly decreased, while GSH administration reversed this change. Our findings suggested that GSH supplementation attenuated overexpressed ONOO(−) from the reaction of excessive NO with and protected against obstructive jaundice-induced vascular hyporesponsiveness in rats.