Perinodopril, an angiotensin converting enzyme inhibitor, attenuates experimental hepatic fibrosis
Shawky, H., Marzouk, S., Obaia, E., Hassouna, A. (2007). Perinodopril, an angiotensin converting enzyme inhibitor, attenuates experimental hepatic fibrosis. EKB Journal Management System, 27(1), 381-392. doi: 10.21608/besps.2007.37175
Heba Shawky; Samar Marzouk; Eman Obaia; Amira Hassouna. "Perinodopril, an angiotensin converting enzyme inhibitor, attenuates experimental hepatic fibrosis". EKB Journal Management System, 27, 1, 2007, 381-392. doi: 10.21608/besps.2007.37175
Shawky, H., Marzouk, S., Obaia, E., Hassouna, A. (2007). 'Perinodopril, an angiotensin converting enzyme inhibitor, attenuates experimental hepatic fibrosis', EKB Journal Management System, 27(1), pp. 381-392. doi: 10.21608/besps.2007.37175
Shawky, H., Marzouk, S., Obaia, E., Hassouna, A. Perinodopril, an angiotensin converting enzyme inhibitor, attenuates experimental hepatic fibrosis. EKB Journal Management System, 2007; 27(1): 381-392. doi: 10.21608/besps.2007.37175

Perinodopril, an angiotensin converting enzyme inhibitor, attenuates experimental hepatic fibrosis

Bulletin of Egyptian Society for Physiological Sciences
Article 24, Volume 27, Issue 1, June 2007, Page 381-392  XML PDF (264.76 K)
Document Type: Original Article
DOI: 10.21608/besps.2007.37175
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Authors
Heba Shawky* 1; Samar Marzouk2; Eman Obaia2; Amira Hassouna2
1Department of Physiology, Faculty of Medicine, Cairo University
2Department of Medical Biochemistry, Faculty of Medicine, Cairo University
Abstract
Liver fibrosis is considered as a progressive pathological process involving multiple
cellular and molecular events that lead to deposition of excess matrix proteins in the extracellular
space. When that process is combined with ineffective regeneration and repair, there is increasing
distortion of the normal liver architecture, and the end result is cirrhosis. Emerging anti-fibrotic
therapies are aimed at inhibiting the accumulation of fibrogenic cells and/or preventing the
deposition of extracellular matrix proteins. Although many therapeutic interventions are effective in
experimental models of liver fibrosis, the mechanisms underlying the anti-fibrotic effect on liver
fibrosis remain unclear. The aim of the present study was to investigate the underlying mechanisms
of anti-fibrotic effect of angiotensin converting enzyme inhibitor (ACEI) on experimental liver
fibrosis induced by carbon tetrachloride (CCl4). Thirty five white albino male rats of 150-200g
average weight were randomly divided into three groups, Group I: The control group (n = 10),
Group II: CCl4 injected rats without any treatment (n = 10) and Group III: CCl4 injected rats that
received an ACEI, perinodopril , dissolved in distilled water, 6mg/kg/day for 4 weeks (n = 15).
Venous blood was collected from retro orbital vein for serum separation for assessment of liver
functions. Liver tissue was subdivided into three portions for: pathological examination, estimation
of transforming growth factor-β1 (TGF-β1) and matrix metalloproteinase-9 (MMP-9) by ELISA and
expression of nuclear factor- kappa beta (NF-κB) in a trial to understand the mechanism underlying
the anti-fibrotic effect of ACEI. Tissue TGF-β1, MMP-9 and NF-κB were significantly higher in
CCl4 group (group II) compared with control group (group I) and they were decreased significantly
with administration of ACEI with CCl4 (group III). In conclusion, ACEI attenuates the progression
of hepatic fibrosis induced by CCl4 by reducing expression of NF-κB, TGF-β1, and MMP- 9.
Keywords
Liver fibrosis; TGF- β1; MMP-9 and NF-κB
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