Lycopene prevents development of steatohepatitis in experimental nonalcoholic steatohepatitis model induced by high-fat diet.

We investigated the preventive effect of lycopene on nonalcoholic steatohepatitis-induced by high-fat diet in rats. Forty male Sprague-Dawley rats were divided into 4 groups. They were fed standard diet, high-fat diet (HFD), high-fat diet plus lycopene at a dose of 2 mg/kg body weight and the high-fat diet lycopene at a dose of 4 mg/kg BW for a period of 6 weeks. Inflammation, steatosis, α-smooth muscle actin (α-SMA), and cytochrome P450 2E1 (CYP 2E1) expression increased significantly in the rats fed HFD and decreased in the rats administered by lycopene. Significantly elevated levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor (TNF α), and serum and liver malondialdehyde (MDA) were observed in rats fed the high-fat diet as compared to the control rats (P < .01). Supplementation with lycopene lowered serum MDA and tumor necrosis factor (TNF-α) levels and elevated liver GSH level (P < .001). Insulin resistance was higher in the rats fed HFD than in rats supplemented with lycopene. The data indicate that supplementation with lycopene can reduce high-fat diet-induced oxidative stress to the cells.

Epigallocatechin gallate attenuates experimental non-alcoholic steatohepatitis induced by high fat diet.

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 < 0.01). Steatosis and inflammation decreased in the HFD + EGCG group, in comparison to the HFD group (P < 0.05, for each). There was a significant decline in ALT (P < 0.01), triglyceride (P < 0.01), insulin (P < 0.05), and glucose (P < 0.05) levels in the HFD + EGCG group, when compared to the HFD group. Plasma and liver MDA levels in the HFD + EGCG group were lower than those of the HFD group; the difference was significant (P < 0.01 for each). Glutathione levels in the HFD + EGCG group was significantly higher those in the HFD group. CYP 2E1 and alpha-smooth muscle actin expression decreased in the HFD + EGCG group, in comparison to the HFD group (P < 0.01, P < 0.05, respectively). CONCLUSION: EGCG reduces the development of experimental non-alcoholic steatohepatitis induced by a high fat diet. It seems to exercise this effect through its effect on lipid metabolism and antioxidant characteristics.

[Biliary fasciolosis: a report of three cases diagnosed by ERCP]. / Biliyer Fasciolosis: ERCP ile Tani Konulan Uç Olgu Raporu.

Fasciola hepatica is an endemic parasite in Turkey. Chronic Fasciola hepatica infestation is known to cause biliary obstruction and inflammation. Also, biliary fasciolosis may be asymptomatic. We report three patients with biliary fasciolosis who were diagnosed and managed by endoscopic retrograde cholangiopancreatography (ERCP). None of cases had eosinophilia. All cases were admitted to hospital with nonspecific symptoms. ERCP may be used for direct diagnosis and management of biliary fasciolosis.

Fasciola hepatica case with hemobilia.

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.

Preventive role of genistein in an experimental non-alcoholic steatohepatitis model.

BACKGROUND AND AIM: 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. METHODS: 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. RESULTS: Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) (P < 0.001 for each), plasma and liver tissue MDA and plasma TNF-alpha levels (P < 0.001, <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 (P > 0.05). Histopathologically, steatosis, inflammatory cells per mm(2) and ballooning degeneration were significantly higher in the placebo group than in the control group (P < 0.001 for each). Nevertheless, AST and ALT (P < 0.05 for each), plasma and liver tissue MDA (P < 0.05 for each) and plasma TNF-alpha levels (P < 0.001) were significantly decreased in the genistein group compared to the placebo group. Histopathologically, steatosis (P < 0.05), inflammatory cells per mm(2) and ballooning degeneration (P < 0.01 for each) in the genistein group were also significantly lower than in the placebo group. CONCLUSIONS: 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.

Protective role of genistein in acute liver damage induced by carbon tetrachloride.

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). Liver tissue MDA level in group 5 was significantly lower than that in group 4 (P < .001). Liver tissue glutathione levels were higher in group 5 and 3, relative to groups 4 and 2, respectively (P > .05 for each). Inflammation and focal necrosis decreased in group 3, in comparison to group 2 (P < .001 for each). Inflammation and focal necrosis in group 5 was lower than that in group 4 (P < .001). Actin expression decreased significantly in group 5, relative to group 4 (P < .05). CONCLUSION: Genistein has anti-inflammatory and antinecrotic effects on experimental liver damage caused by CCl4. Genistein reduces liver damage by preventing lipid peroxidation and strengthening antioxidant systems.

Amelioration of steatohepatitis with pentoxifylline in a novel nonalcoholic steatohepatitis model induced by high-fat diet.

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.

The levels of ghrelin, leptin, TNF-alpha, and IL-6 in liver cirrhosis and hepatocellular carcinoma due to HBV and HDV infection.

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-alpha, IL-6 and the severity of the disease. MATERIALS AND METHODS: We measured serum ghrelin, leptin, TNF-alpha, 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-alpha, 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-alpha, and a negative correlation between leptin and TNF-alpha (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-alpha. The presence of nutritional and metabolic abnormalities, including malnutrition, in cirrhosis and HCC may, at least partly, elucidate high ghrelin and low leptin levels.