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 2mg/kg body weight and the high-fat diet lycopene at a dose of 4mg/kg BW for a period of 6 weeks. Inflammation, steatosis, -smooth muscle actin (-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 ), and serum and liver malondialdehyde (MDA) were observed in rats fed the high-fat diet as compared to the control rats (). Supplementation with lycopene lowered serum MDA and tumor necrosis factor (TNF-) levels and elevated liver GSH level (). 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.

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.

Background: The only established therapy for chronic viral delta hepatitis, the most severe form of viral hepatitis is treatment with pegylated-interferon α (Peg IFN α). Objectives: In this study, we aimed to determine the efficacy of pegylated-interferon α 2a (Peg-IFN α 2a) and 2b (Peg IFN α 2b) in the treatment of patients infected with chronic delta hepatitis virus. Patients and Methods: The sample size was based on available patients potentially to be recruited. Data of 63 patients receiving either Peg IFN alpha 2a or Peg IFN alpha 2b were retrospectively assessed in the present cohort study performed in Turkey. Of 56 patients completed the study, 41 received Peg IFN α 2a and 15 received Peg IFN α 2b for 12 months. Patients were evaluated for biochemical and virological responses at the end of given treatment and six months after the treatment. Results: Stage of fibrosis was found high in both groups (85.4% vs. 86.7%), while cirrhosis was higher in the group of Peg IFN α 2b (53.3% vs. 34.1%). At the end of treatment, either hepatitis delta virus RNA (HDV RNA) alone or both HDV RNA and hepatitis b virus DNA (HBV DNA) had negative results in 32% of patients. Although HDV RNA negativity was sustained in 30.3% of patients, negativity of both HDV RNA and HBV DNA was decreased to 19.6% six months after completion of the treatment. HBV DNA became positive in one third of patients with response at six months after completion of the treatment (10.7% of all patients). HDV RNA negativity at month six was found as a predictor of positive response. No significant difference was found between Peg IFN α 2a and Peg IFN α 2b for virological response rate. Conclusions: Treatment with Peg IFN α achieved a sustained negativity of HDV RNA in about one third of patients. Duration of Peg IFN α therapy might be prolonged to at least 24 months or more to prevent the occurrence of Hepatitis B virus (HBV) relapse encountered six months after completion of the treatment. Keywords: Hepatitis D; Interferon; Therapeutics

Introduction: In the context of the present study, we have aimed to examine the effects of the administration of whey protein through rectal enema to a acetic acid-induced ulcerative colitis in rats on the pathways of nuclear-related factor-2 (Nrf-2), heme oxygenase-1 (HO-1), nuclear factor kappa B (NF-κB), active protein kinase-1 (AP-1), tumour necrotising factor-alpha (TNF-α), and cyclooxygenase-2 (COX-2), IL-6, IL-10.Material and methods: 28 rats were employed for the trial. Ulcerative colitis was induced through the use of acetic acid. The therapeutic doses of whey protein were administered rectally. Ulcerative colitis was made subject to histopathological examination and protein levels in colon tissue measured with the Western Blot Method.Results: The significant increases observed in the levels of AP-1, COX-2, IL-6, IL-10, NF-κβ, and TNF-α as markers of inflammation following the development of ulcerative colitis enjoyed remarkable decreases along with the administration of whey protein (p<0.05). On the other hand, we identified a decrease in the Nrf2-ARE signal pathway and HO-1 protein assuming protective roles on the colon inflammatory response along with the development of ulcerative colitis and an activation of the Nrf2-HO-1 pathway by the whey protein.Conclusions: Whey protein modulates Nrf2/HO-1 and NF-kB pathways, thereby creating a therapeutic effect against colonic inflammation induced by acetic acid (AA) by reason of its anti-inflammatory implications.