Role of selenium in protection of liver cirrhosis

Selenium is an essential trace element and has been shown to protect the rats against dietary liver necrosis. This study was designed to evaluate the effects of selenium supplementation on different biochemical parameters in thioacetamide induced cirrhotic rats. For this purpose 24 male Albino wistar rats were divided into four groups [n=6]. Group 1, remained healthy control rats, Group 2, received thioacetamide [at a dose of 200mg/kg b.w, i.p, for 12 weeks, twice a week] in first phase and saline in second phase, Group 3, received thioacetamide [200mg/kg b.w, i.p for 12 weeks, twice a week] in first phase and sodium selenite [1mg/kg b.w, i.p. for 12 weeks, three times a week] in second phase and Group 4, received sodium selenite [1mg/kg b.w, i.p. for 12 weeks, three times a week] in first phase and saline in second phase. Biochemical analysis was evaluated by total and direct bilirubin, liver specific enzymes, and antioxidant enzymes. Marked increase in total and direct bilirubin and ALT activity was the indicative markers of liver cirrhosis while reduced antioxidant activity [SOD and GSH] and increased MDA and Catalase levels were observed in cirrhotic group. Sodium selenite supplementation markedly reduced total bilirubin and ALT activity and restored the antioxidant enzymes [SOD and GSH] and MDA and catalase activity. These results indicate that sodium selenite successively attenuates the thioacetamide induced liver cirrhosis

Angiotensin converting enzyme [ACE] gene expression in experimentally induced liver cirrhosis in rats

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