The Role of e-NOS in Chronic Cholestasis-Induced Liver and Renal Injury in Rats: The Effect of N-Acetyl Cysteine
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....
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doaj-cfa3a8f44a21465087b4c5a8eb54c27b2020-11-24T20:59:11ZengHindawi LimitedGastroenterology Research and Practice1687-61211687-630X2014-01-01201410.1155/2014/564949564949The Role of e-NOS in Chronic Cholestasis-Induced Liver and Renal Injury in Rats: The Effect of N-Acetyl CysteineYusuf Gunay0Semsi Altaner1Nergiz Ekmen2Department of Surgery, Atakent Hospital, Acibadem University, Halkali, 34678 Istanbul, TurkeyDepartment of Pathology, Baskent University Istanbul Hospital, Altunizade, 34567 Istanbul, TurkeyDepartment of Gastroenterology, Florence Nightingale Hospital, Bilim University, Sisli, 34321 Istanbul, TurkeyIntroduction. 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%, P=.025), but the intensity of e-NOS in liver was lower in rats that received NAC (1.3 versus 2.7, P=.046). The necrotic area in the kidneys among rats that received NAC was lower at week 4 (48% versus 57%; P<.001). 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.http://dx.doi.org/10.1155/2014/564949 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Yusuf Gunay Semsi Altaner Nergiz Ekmen |
spellingShingle |
Yusuf Gunay Semsi Altaner Nergiz Ekmen The Role of e-NOS in Chronic Cholestasis-Induced Liver and Renal Injury in Rats: The Effect of N-Acetyl Cysteine Gastroenterology Research and Practice |
author_facet |
Yusuf Gunay Semsi Altaner Nergiz Ekmen |
author_sort |
Yusuf Gunay |
title |
The Role of e-NOS in Chronic Cholestasis-Induced Liver and Renal Injury in Rats: The Effect of N-Acetyl Cysteine |
title_short |
The Role of e-NOS in Chronic Cholestasis-Induced Liver and Renal Injury in Rats: The Effect of N-Acetyl Cysteine |
title_full |
The Role of e-NOS in Chronic Cholestasis-Induced Liver and Renal Injury in Rats: The Effect of N-Acetyl Cysteine |
title_fullStr |
The Role of e-NOS in Chronic Cholestasis-Induced Liver and Renal Injury in Rats: The Effect of N-Acetyl Cysteine |
title_full_unstemmed |
The Role of e-NOS in Chronic Cholestasis-Induced Liver and Renal Injury in Rats: The Effect of N-Acetyl Cysteine |
title_sort |
role of e-nos in chronic cholestasis-induced liver and renal injury in rats: the effect of n-acetyl cysteine |
publisher |
Hindawi Limited |
series |
Gastroenterology Research and Practice |
issn |
1687-6121 1687-630X |
publishDate |
2014-01-01 |
description |
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%, P=.025), but the intensity of e-NOS in liver was lower in rats that received NAC (1.3 versus 2.7, P=.046). The necrotic area in the kidneys among rats that received NAC was lower at week 4 (48% versus 57%; P<.001). 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. |
url |
http://dx.doi.org/10.1155/2014/564949 |
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