Person: EREN, FATİH
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EREN
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FATİH
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Publication Open Access Adrenomedullin in cirrhotic and non-cirrhotic portal hypertension(2003) EREN, FATİHPublication Metadata only Iron preloading aggravates nutritional steatohepatitis in rats by increasing apoptotic cell death(ELSEVIER, 2007) EREN, FATİH; Imeryuz, Nese; Tahan, Veysel; Sonsuz, Abdullah; Eren, Fatih; Uraz, Suleyman; Yuksel, Meral; Akpulat, Sertac; Ozcelik, Dervis; Haklar, Goncagul; Celike, Cigdem; Avsar, Erol; Tozun, NurdanBackground/Aims: High serum ferritin and liver iron concentrations were found in some patients with NASH, suggesting a role for iron as a co-factor that aggravates liver injury. The aim of this study is to investigate the effects of parenteral iron in a rat model of NASH induced by a methionine choline deficient diet (MCDD). Methods:Wistar rats were divided into 1 - Control, 2 - Iron (Fe), 3 - MCDD, 4 - MCDD&Fe groups. Iron dextran 100 mg/kg was administered intra-muscularly in groups 2 and 4. All rats were fed MCDD, Groups I and 2 were supplied with choline and methionine. Blood and tissue samples were obtained after 4 weeks. Results: The iron injection alone did not affect the liver whereas MCDD led to steatohepatitis. Iron worsened steatosis without any obvious effect on accompanying inflammation. It aggravated tissue injury by increasing apoptosis. Liver fibrosis was observed only in 3 out of 10 rats in the MCDD&Fe group. Conclusions: Observation of liver fibrosis only in the MCDD&Fe group suggests that iron induced increase in apoptosis contributes to the development of fibrosis at an earlier time than expected. (c) 2007 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.Publication Metadata only The effects of N-Acetylcysteine on bile duct ligation-induced liver fibrosis in rats(SPRINGER, 2007) EREN, FATİH; Tahan, Gulgun; Tarcin, Orhan; Tahan, Veysel; Eren, Fatih; Gedik, Nursal; Sahan, Elife; Biberoglu, Nilgun; Guzel, Savas; Bozbas, Aysun; Tozun, Nurdan; Yucel, OsmanStellate cells are activated by free radicals, and synthesize collagen. N-acetylcysteine (NAC) is a precursor of reduced glutathione and a potent scavenger of hydroxyl radicals and has potential antifibrotic effects. We aimed to test the effects of NAC on bile duct ligation (BDL) induced liver damage in rats. Forty-seven Wistar rats were divided into 5 groups: group 1, BDL + NAC (n = 10); group 2, BDL (n = 10); group 3, sham + NAC (n = 10); group 4, sham (n = 10); and group 5, control group (n = 10). NAC (50 mu mol/kg per day) or saline of single doses were administered intraperitoneally for 28 days. Serum biochemical and liver oxidative stress parameters were studied. Liver collagen level was determined by the method of Lopez de Leon and Rojkind. Liver slides were stained by hematoxylin and eosin and Masson trichrome\Gomory reticulum staining. Aspartate aminotransferase (AST) and alkaline phosphatase levels in the BDL + NAC group were lower than the BDL group and were higher than the control groups (all P < .001). Malondialdehyde, luminal, and glutathione levels in group 1 were lower than the BDL group (P = .01, P = .002, and P < .001) and higher than the control groups (all P < .001). NAC had no effect on alanine aminotransferase (ALT), gammaglutamyl transferase, bilirubin, albumin, or lucigenin levels. Liver collagen levels were higher in the BDL groups (P < .001); however, NAC had no effect on the collagen levels. The BDL groups showed stage 3 fibrosis; all the control groups were normal. NAC improved some biochemical parameters (AST, alkaline phosphatase) and oxidative stress parameters (malondialdehyde, luminol, glutathione) in the BDL model. NAC was found to be effective on cholestasis-induced hepatotoxicity. However, NAC was inefficient as an antifibrotic agent within a 1-month period of administration in the BDL model.Publication Metadata only Serum Levels of Adipokines in Patients with Chronic HCV Infection: Relationship with Steatosis and Fibrosis(ELSEVIER SCIENCE INC, 2009) ÇELİKEL, ÇİĞDEM; Tiftikci, Arzu; Atug, Ozlen; Yilmaz, Yusuf; Eren, Fatih; Ozdemir, Filiz Ture; Yapali, Suna; Ozdogan, Osman; Celikel, Cigdem Ataizi; Imeryuz, Nese; Tozun, NurdanBackground and Aims. Hepatic steatosis and fibrosis are common histological findings in patients with chronic hepatitis C virus (HCV) infection. In this study we sought to determine whether serum levels of three adipokines (leptin, adiponectin and resistin) show any biochemical correlation with hepatic steatosis and fibrosis in patients with chronic HCV infection. Methods. We examined a total of 51 patients with chronic HCV infection (22 males and 29 females, mean BMI: 27.4 +/- 5 kg/m(2)) and 24 healthy control subjects (10 males and 14 females, mean BMI: 23.2 +/- 3 kg/m(2)). Liver steatosis and fibrosis were scored on biopsies. Serum levels of leptin, adiponectin and resistin were determined by ELISA. Results. HCV genotypes were 1b in 41 patients (80.4%), 3a in three patients (5.9%), 2a in two patients (3.9%), 1 a in two patients (3.9%), 1 c in one patient (2%), and 2b in one patient (2%). Serum levels of leptin, resistin, and the leptin-to-adiponectin ratio were significantly higher in patients with chronic HCV infection than in controls. Steatosis and fibrosis were detected in 33.3% and 70.5% of chronic HCV patients, respectively. No significant association with serum adipokine levels and degree of steatosis was evident. Low serum levels of resistin were associated with the presence of fibrosis independently of potential confounders. Conclusions. Patients with chronic HCV infection display elevated levels of adipokines in their sera. Reduced concentrations of resistin may be a biochemical marker of fibrosis in this patient group. (C) 2009 IMSS. Published by Elsevier Inc.Publication Metadata only Rosiglitazone attenuates liver inflammation in a rat model of nonalcoholic steatohepatitis(SPRINGER, 2007) ÇELİKEL, ÇİĞDEM; Tahan, Veysel; Eren, Fatih; Avsar, Erol; Yavuz, Dilek; Yuksel, Meral; Emekli, Ebru; Imeryuz, Nese; Celikel, Cigdem; Uzun, Hafize; Haklar, Goncagul; Tozun, NurdanRosiglitazone is an insulin-sensitizing agent. We aimed to assess the effects of rosiglitazone on a methionine- and choline-deficient diet (MCDD) model of nonalcoholic steatohepatitis (NASH) in rats. Wistar rats were fed either MCDD or a control diet in the 4-week induction study; they were given saline or 4 mg/kg/day rosiglitazone. After the induction study period, the rats were divided into four groups and fed MCDD or given a control diet for an additional 8 weeks and received saline or rosiglitazone. Serum and tissue samples were obtained. Rosiglitazone improved inflammation in NASH and improved ALT, alkaline phosphatase, and interleukin-6 levels in the induction study and interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha levels in the treatment study. Our preliminary study is the first to show the anti-inflammatory effects of rosiglitazone in NASH. Rosiglitazone's effect on cytokines may be a key mechanism of its anti-inflammatory effect in NASH.Publication Metadata only Role of ursodeoxycholic acid in prevention of methotrexate-induced liver toxicity(SPRINGER, 2008) ÇELİKEL, ÇİĞDEM; Uraz, Suleyman; Tahan, Veysel; Aygun, Cem; Eren, Fatih; Unluguzel, Goksenin; Yuksel, Meral; Senturk, Omer; Avsar, Erol; Haklar, Goncagul; Celikel, Cigdem; Hulagu, Sadettin; Tozun, NurdanAim Methotrexate (MTX)-induced hepatotoxicity restricts the clinical use of this immunosuppressive drug. In this study, our aim was to research the role of oxidative stress in the hepatic toxicity of MTX and the protective effect of ursodeoxycholic acid (UDCA) in this setting. Methods Wistar type rats (n = 32) were divided into four groups; group-1 as the MTX + UDCA, group-2 as the MTX, group-3 as the UDCA, group-4 as the saline-receiving groups. The MTX + UDCA and MTX groups of rats received 50 mg/kg of UDCA administered orally; whilst physiological saline was administered orally to the MTX and saline groups and continued for the next 6 days. On the second day of the study, the MTX + UDCA and MTX groups had a single intraperitoneal dose of MTX of 20 mg/kg. The UDCA and saline groups also received similar volumes of physiological saline intraperitoneally. On the sixth day, serum samples were collected and analyzed for ALT, alkaline phosphatase (ALP) and gamma glutamyl transpeptidase (GGT) and homogenated liver tissues were examined for reactive oxygen metabolites (ROM); luminol, lucigenin, lipid peroxygenation product malondialdehyde (MDA) and glutathione (GSH) levels. Results In the MTX group, serum ALT, ALP, GGT and tissue ROM levels were higher and GSH level was lower. On the histopathological examination, hepatocellular necrosis was clearly more evident in the MTX group than the MTX + UDCA group. Conclusions UDCA treatment protects against MTX-induced liver toxicity. Histopathologically hepatocyte necrosis can be prevented by UDCA treatment, indicating clearly the hepatoprotective effect of this agent on MTX-induced liver injury.