Antioxidants vitamin E and C attenuate hepatic fibrosis in biliary-obstructed rats

AIM： To investigate whether antioxidants vitamin E and C can retard development of hepatic fibrosis in the bilian/obstructed rats. METHODS： Fifty Wistar albino rats were randomly assigned to 5 groups （10 rats in each）. Bile duct was ligated in 40 rats and they were treated as follows： group vitC, vitamin C 10 mg/kg sc daily; group vitE, vitamin E 15 mg/kg sc daily; group vitEC, both of the vitamins; bile duct-ligated （BDL, control） group, physiological saline sc. The fifth group was assigned to sham operation. At the end of fourth week, the rats were decapitated, and hepatic tissue biochemical collagen content and collagen surface area were measured. Hepatic tissue specimens were histopathologically evaluated according to Scheuer system. Serum hyaluronate levels were measured by ELISA method. RESULTS： Despite being higher than sham group, hepatic collagen level was significantly decreased in each of the vitC, vitE and vitEC groups （32.7 ± 1.2, 33.8 ± 2.9, 36.7 ± 0.5 ）μg collagen/mg protein, respectively） compared to BDL （48.3 ± 0.6 mg collagen/g protein） （P 〈 0.001 for each vitamin group）. Each isolated vitamin C, isolated vitamin E and combined vitamin E/C supplementation prevented the increase in hepatic collagen surface density （7.0% ± 1.1%, 6.2% ± 1.7%, 12.3% ± 2.0%, respectively） compared to BDL （17.4% ± 5.6%） （P 〈 0.05 for each）. The same beneficial effect of vitamin C, vitamin E and combined vitamin E/C treatment was also observed on the decrease of serum hyaluronate levels compared to BDL group （P 〈 0.001）. The relative liver and spleen weights, serum transaminases, cholestatic enzymes, bilirubins and histopathological inflammation scores were not different between the antioxidant treatment groups and the control. However, fibrosis staging scores were obviously reduced only in the vitamin E/C combination group （vit EC： 2.4 ± 0.8 vs BDL： 3.1 ± 0.7; P 〈 0.05）. CONCLUSION： Each antioxidant vitamin E, vitamin C and their combination retard hepatic fibrosis in biliary-obstructed rats. Oxidative stress may play a role in the pathogenesis of hepatic fibrosis in secondary biliary cirrhosis.

Heart Valve Lesions Due to the Formation of a Beta-Hemolytic Streptococ Role of Adhesion Molecules

Objectives: A rise in the levels of adhesion molecules such as VCAM-1, ICAM-1and E-selectin in valve disease patients has been reported lately. In our study, by detecting the presence of adhesion molecule expression in the valve endothelium we will try to show the level of adhesion molecules in peripheral blood leucocytes. Materials and Methods: Valve samples were obtained from patients having undergone aortic and mitral valve replacement due to symptomatic aortic stenosis/aortic insufficiency and/or mitral stenosis/mitral insufficiency. The clinical preoperative diagnosis was made using two-dimensional echocardiography and Doppler echocardiography. Rheumatic valves were in group B (n = 20). Group A (n = 8) constituted the control group. Immunohistochemical staining was performed using CD4, CD8, CD54/ICAM-1, and CD106/VCAM-1. Flow cytometric analysis was performed. The Kolmogorov-Smirnov test and Fisher’s exact test were used for the comparison of categorical variables. Results: Group A (non-rheumatic) patients were found to be older than group B (rheumatic) patients (59.8 ± 11.4 years vs. 45.3 ± 11.8 years, p = 0.008). In group B VCAM-1 level was higher than that of group A (296.6 ± 21.2 vs. 258.5 ± 42.1, p = 0.004). CD11b monocyte in group B was higher than in group A (98.8 ± 0.5 vs. 92.9 ± 9.7, p = 0.003). CD11b granulocyte was higher in group B than in group A (99.96 ± 0.05 vs. 93.79 ± 13.26, p = 0.33). Significant differences were not determined in the other parameters. Conclusion: The fact that increases in serum VCAM-1 and CD-11b only occurred in patients with rheumatic valvular disease in our study suggests that inflammation in patients with the same hemodynamic disorder is higher in rheumatic valvular disease than in the ones with non-rheumatic valvular disease.