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Angiotensin-converting enzyme inhibitor prevents oxidative stress, inflammation, and fibrosis in carbon tetrachloride-treated rat liver.

Authors
  • Reza, Hasan Mahmud1
  • Tabassum, Nabila1
  • Sagor, Md Abu Taher1
  • Chowdhury, Mohammed Riaz Hasan1
  • Rahman, Mahbubur1
  • Jain, Preeti1
  • Alam, Md Ashraful1
  • 1 a Department of Pharmaceutical Sciences , School of Health and Life Science, North South University Bangladesh , Bashundhara , Dhaka , Bangladesh. , (Bangladesh)
Type
Published Article
Journal
Toxicology Mechanisms and Methods
Publisher
Informa UK (Taylor & Francis)
Publication Date
2016
Volume
26
Issue
1
Pages
46–53
Identifiers
DOI: 10.3109/15376516.2015.1124956
PMID: 26862777
Source
Medline
Keywords
License
Unknown

Abstract

Hepatic fibrosis is a common feature of chronic liver injury, and the involvement of angiotensin II in such process has been studied earlier. We hypothesized that anti-angiotensin II agents may be effective in preventing hepatic fibrosis. In this study, Long Evans female rats were used and divided into four groups such as Group-I, Control; Group-II, Control + ramipril; Group-III, CCl4; and Group-IV, CCl4 + ramipril. Group II and IV are treated with ramipril for 14 d. At the end of treatment, the livers were removed, and the level of hepatic marker enzymes (aspartate aminotransferase, Alanine aminotransferase, and alkaline phosphatase), nitric oxide, advanced protein oxidation product , catalase activity, and lipid peroxidation were determined. The degree of fibrosis was evaluated through histopathological staining with Sirius red and trichrome milligan staining. Carbon-tetrachloride (CCl4) administration in rats developed hepatic dysfunction and raised the hepatic marker enzymes activities significantly. CCl4 administration in rats also produced oxidative stress, inflammation, and fibrosis in liver. Furthermore, angiotensinogen-inhibitor ramipril normalized the hepatic enzymes activities and improved the antioxidant enzyme catalase activity. Moreover, ramipril treatment ameliorated lipid peroxidation and hepatic inflammation in CCl4-treated rats. Ramipril treatment also significantly reduced hepatic fibrosis in CCl4-administered rats. In conclusion, our investigation suggests that the antifibrotic effect of ramipril may be attributed to inhibition of angiotensin-II mediated oxidative stress and inflammation in liver CCl4-administered rats.

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