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Gastroenterology Research and Practice
Volume 2014, Article ID 564949, 8 pages
Research Article

The Role of e-NOS in Chronic Cholestasis-Induced Liver and Renal Injury in Rats: The Effect of N-Acetyl Cysteine

1Department of Surgery, Atakent Hospital, Acibadem University, Halkali, 34678 Istanbul, Turkey
2Department of Pathology, Baskent University Istanbul Hospital, Altunizade, 34567 Istanbul, Turkey
3Department of Gastroenterology, Florence Nightingale Hospital, Bilim University, Sisli, 34321 Istanbul, Turkey

Received 13 July 2014; Revised 20 October 2014; Accepted 21 October 2014; Published 9 November 2014

Academic Editor: Michel Kahaleh

Copyright © 2014 Yusuf Gunay 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.


Introduction. The role of chronic cholestasis (CC) in liver injury and fibrosis remains unclear. The aims of this study were to define the role of endothelial nitric oxide synthase (e-NOS) in CC and the protective effect of N-acetyl-L-cysteine (NAC) in liver and kidney injury. Materials and Methods. Group A (sham group); Group B (CBDL); and Group C (CBDL + NAC). Group C received daily dosage of NAC (100 mg/kg) intraperitoneally for up to 4 weeks. Results. The rate of bridging fibrosis was higher (100% versus 20%, ), but the intensity of e-NOS in liver was lower in rats that received NAC (1.3 versus 2.7, ). The necrotic area in the kidneys among rats that received NAC was lower at week 4 (48% versus 57%; ). The numbers of e-NOS stained cells in kidney were similar in sham group and the two groups with CBDL. Discussion. NAC reduced the stimulus for liver fibrosis in this rat model of CC and attenuated liver and kidney injury. Our study showed that e-NOS expression increased in liver tissue of rats with CC and that this was reversed by NAC. Treatment with NAC might restore e-NOS protein expression and prevent liver injury in CC.