Abstract:
Angiotensin converting enzyme (ACE) is a key player of Renin Angiotensin System (RAS), involved in
conversion of active product, angiotensin-II. Alterations in RAS have been implicated in the pathophysiology of various diseases involving heart, kidney, lung and liver. This study is designed to investigate the association of ACE gene expression in induction of liver cirrhosis in rats. Total 12 male albino Wistar rats were selected and divided in two groups. Control group received 0.9% NaCl, where as Test group received thioacidamide (TAA), dissolved in 0.9%NaCl, injected intraperitoneally at a dosage of 200mg/Kg of body weight, twice a week for 12 weeks. The rats were decapitated and blood sample was collected at the end of experimental period and used for liver functions, enzyme activity, antioxidant enzymes and lipid peroxidation estimations. Genomic DNA was isolated from excised tissue determine the
ACE genotypes using specific primers. The ACE gene expression in liver tissue was assessed using the quantitative RTPCR method. The activity of ALT, total and direct bilirubin, SOD and CAT levels were significantly high (p<0.05) and
level of MDA was significantly low (p<0.05) in TAA treated rats as compared to control rats. The ACE gene expression
after 12 weeks TAA treatment in cirrhotic rats was significantly increased (p<0.05) in comparison to controls. This study
describes the importance of RAS in the development of hepatic fibrosis and the benefits of modulation of this system
ACE gene expression. The finding of major up-regulation of ACE in the experimental rat liver provides further insight
into the complexities of the RAS and its regulation in liver injury. The development of specific modulators of ACE
activity and function, in future, will help determine the role of ACE and its genetic variants in the pathophysiology of
liver disease
