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We sought to evaluate the effects of pentoxifylline (PTX) on steatohepatitis in a novel experimental nonalcoholic steatohepatitis (NASH) model induced by a high-fat diet (HFD). Thirty-three male Sprague-Dawley rats were randomly divided into 3 groups. The first group received only standard rat diet (control group); groups 2 (placebo group) and 3 were given HFD, ad libitum. After week 4, 0.5 mL of physiologic serum was injected subcutaneously to the placebo group and 50 mg/kg/d PTX was given intraperitoneally to the third group (group PTX). After 6 weeks all rats were humanely killed. Serum biochemistry, tumor necrosis factor-alpha (TNF-alpha), plasma, and liver tissue malondialdehyde (MDA) were analyzed. Histopathologically, steatosis, ballooning degeneration, inflammation, and fibrosis were determined. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, plasma and liver tissue MDA, and plasma TNF-alpha levels were significantly higher in placebo group than in the control group. Tumor growth factor-beta levels, however, were comparable in the placebo and control groups. On histopathologic examination, steatosis, inflammatory cells per square millimeter, and ballooning degeneration were significantly higher in the placebo group than in the control group. No fibrosis or Mallory bodies were found in the placebo group. AST, ALT, plasma and liver tissue MDA, and plasma TNF-alpha levels were significantly lower in PTX group compared to the placebo group. Histopathologically, steatosis, mean number of inflammatory cells/mm(2) and ballooning degeneration in PTX group were also significantly lower than in the placebo group. In conclusion, PTX strikingly ameliorates steatohepatitis in this novel NASH model not only by inhibiting the TNF-alpha but also suppressing the oxidative stress markers.

Background/Aim. Malnutrition, a common problem in liver cirrhosis and HCC, may readily deteriorate the clinical functions with resultant poor prognosis. Beside the hyper catabolic state frequently encountered in chronic liver disease and HCC, anorexia and reduced food intake also worsen the malnutrition. The recently discovered peptide hormone ghrelin acts as a counterpart of leptin in regulation of food intake and fat utilization. The aim of the present study was to investigate the ghrelin and leptin levels in cirrhosis and HCC due to hepatitis B and D viruses, and the association of ghrelin and leptin with TNF-α, IL-6 and the severity of the disease. Materials and methods. We measured serum ghrelin, leptin, TNF-α, and IL-6 levels using specific immunoassay in 45 patients (23 cirrhosis, 22 HCC) with HBV and/or HDV and in 25 control subjects. Results. In comparison to controls, serum ghrelin, TNF-α, and IL-6 levels were significantly higher in cirrhosis and HCC (P < .05), whereas serum leptin levels were found decreased (P < .05). There was a positive correlation between ghrelin and TNF-α, and a negative correlation between leptin and TNF-α (P < .05). Conclusion. In cirrhosis and HCC due to HBV or HDV, serum ghrelin levels were increased with a corresponding decrease in serum leptin concentrations, acting as a physiological counterpart of ghrelin. The increasing of ghrelin is more prominent in Child C cirrhosis and the level was correlated with TNF-α. The presence of nutritional and metabolic abnormalities, including malnutrition, in cirrhosis and HCC may, at least partly, elucidate high ghrelin and low leptin levels.

The aim of the present study was to evaluate the preventive role of genistein, a phytoestrogen with a wide variety of pharmacological effects, in an experimental non-alcoholic steatohepatitis (NASH) model.Thirty-six Sprague-Dawley rats were divided into three groups. Group 1 (control) received only a standard rat diet, group 2 (placebo) was given a high fat diet (HFD) plus 0.5 mL/day saline subcutaneously, and group 3 (genistein group) a HFD plus subcutaneous genistein injection at dose of 0.2 mg/kg/day for 6 weeks. All rats were killed after 6 weeks. Serum aminotransferases, tumor necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta, and plasma and liver malondialdehyde (MDA) levels were measured. Additionally, steatosis, ballooning degeneration and inflammation of the liver were examined histopathologically.Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) (P0.001 for each), plasma and liver tissue MDA and plasma TNF-alpha levels (P0.001,0.001,0.01, respectively) were found to be higher in the placebo group than in the control group. TGF-beta levels, however, were comparable in the placebo and control groups (P0.05). Histopathologically, steatosis, inflammatory cells per mm(2) and ballooning degeneration were significantly higher in the placebo group than in the control group (P0.001 for each). Nevertheless, AST and ALT (P0.05 for each), plasma and liver tissue MDA (P0.05 for each) and plasma TNF-alpha levels (P0.001) were significantly decreased in the genistein group compared to the placebo group. Histopathologically, steatosis (P0.05), inflammatory cells per mm(2) and ballooning degeneration (P0.01 for each) in the genistein group were also significantly lower than in the placebo group.Genistein, a strong antioxidant agent, significantly decreased the plasma TNF-alpha level and remarkably prevented the emergence of NASH by improving the biochemical and histopathological abnormalities via attenuating oxidative stress.

Background and Aim: In the present study, we examined the preventive role of epigallocatechin gallate (EGCG) in an experimental non-alcoholic steatohepatitis model induced by a high fat diet. Methods: The study included 21 male Sprague-Dawley rats, which were equally divided into three groups. The first group was fed on a standard rat diet, the second group on a high fat diet (HFD), and the third group on a HFD + EGCG. The study concluded after 6 weeks. Histopathological examination was performed. Plasma and tissue MDA levels, glucose, insulin, alanine aminotransferase (ALT), aspartate aminotransferase, gamma glutamyltransferase, alkaline phosphatase, triglyceride, and cholesterol levels were studied. Insulin resistance was calculated by the homeostasis model of insulin resistance method. Results: Steatosis, inflammation, ballooning degeneration, and necrosis increased significantly in the HFD group, compared to the control group (P

Aim. In the present study, we investigated the protective effect of genistein in experimental acute liver damage induced by CCl4. Method. Forty rats were equally allocated to 5 groups. The first group was designated as the control group (group 1). The second group was injected with intraperitoneal CCl4 for 3 days (group 2). The third group was injected with subcutaneous 1 mg/kg genistein for 4 days starting one day before CCl4 injection. The fourth group was injected with intraperitoneal CCl4 for 7 days. The fifth group was injected with subcutaneous 1 mg/kg genistein for 8 days starting one day before CCl4 injection. Plasma and liver tissue malondialdehyde (MDA) and liver glutathione levels, as well as AST and ALT levels were studied. A histopathological examination was conducted. Results. Liver tissue MDA levels were found significantly lower in group 3, in comparison to group 2 (P.05 for each). Inflammation and focal necrosis decreased in group 3, in comparison to group 2 (P

Fasciola hepatica (FH) can lead to important hepatobiliary diseases. Here we present a case of hemobilia associated with biliary FH, which is quite a rare case. The 41–year-old patient, who underwent common bile duct exploration due to hemobilia, was found to have arterial bleeding associated with ulcer caused by a dead parasite in the common bile duct. Hemobilia is a very rare complication associated with FH. When searching for the cause of hemobilia, FH should be considered.