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Öğe An antibody of TNF-alpha did not prevent thioacetamide-induced hepatotoxicity in rats(Sage Publications Ltd, 2011) Demirel, Ulvi; Harputluoglu, Murat M. M.; Seckin, Yuksel; Ciralik, Harun; Temel, Ismail; Ozyalin, Fatma; Otlu, BarisTumor necrosis factor (TNF)-alpha antibodies have been shown to reduce liver damage in different models. We investigated the effects of infliximab (a TNF-alpha antibody) on liver damage in thioacetamide (TAA)-induced hepatotoxicity in rats. Group 1 (n = 8) was the control group. In group 2 (n = 8), the TAA group, the rats received 300 mg/kg intraperitoneal (ip) TAA daily for 2 days. In group 3 (n = 8), the TAA + Infliximab (INF) group, infliximab (5 mg/kg ip daily) was administered 48 hours before the first dose of TAA daily for 2 days and was maintained for 4 consecutive days. In group 4 (n = 8), the INF group, the rats received only ip infliximab (5 mg/kg) daily. Livers were excised for histopathological and biochemical tests (thiobarbituric-acid-reactive substances [TBARS], and myeloperoxidase [MPO]). Serum ammonia, aspartate transaminase (AST), alanine transaminase (ALT), TNF-alpha, liver TBARS and MPO levels, and liver necrosis and inflammation scores in the TAA group were significantly higher than in the control and INF groups (all p < 0.01). All parameters except AST were not significantly different between TAA and TAA + INF. In conclusion, our results suggest that oxidative stress plays an important role in TAA-induced hepatotoxicity, and infliximab does not improve oxidative liver damage.Öğe Effects of Rifaximin on Bacterial Translocation in Thioacetamide-Induced Liver Injury in Rats(Springer/Plenum Publishers, 2012) Harputluoglu, Murat M. M.; Demirel, Ulvi; Gul, Mehmet; Temel, Ismail; Gursoy, Sule; Selcuk, Engin Burak; Aladag, MuratIntestinal bacterial overgrowth (IBO) and increased mucosal permeability are suggested to increase bacterial translocation (BT) in liver injury. Rifaximin (RIF) is a minimally absorbed oral antimicrobial agent that restores gut microflora imbalance. The aim of the present study was to investigate the effects of RIF on BT frequency in thioacetamide (TAA)-induced liver injury. Group 1 was the control. In group 2 (TAA), rats received TAA daily for 3 days. In group 3 (TAA + RIF), RIF was commenced on the same day as the first dose of TAA. In group 4 (RIF), rats received only RIF. Ileal aspirate Escherichia coli counts were significantly lower in the TAA + RIF group than in TAA group. There was no difference in BT frequency between the TAA and TAA + RIF groups. Our results suggest that factors such as intestinal barrier dysfunction and impaired host immune shield, apart from IBO, play an important role in BT in this model.Öğe NOD2 Risk Variants and Pathological Bacterial Translocation in Decompensated Cirrhosis Reply(Springer, 2016) Harputluoglu, Murat M. M.; Bilgic, Yilmaz; Erdogan, Mehmet Ali; Atayan, Yahya; Cagin, Yasir Furkan; Dertli, Ramazan; Otlu, Baris[Abstract Not Available]Öğe Nucleotide-Binding Oligomerization Domain-Containing Protein 2 Variants in Patients with Spontaneous Bacterial Peritonitis(Springer, 2016) Harputluoglu, Murat M. M.; Dertli, Ramazan; Otlu, Baris; Demirel, Ulvi; Yener, Ozkan; Bilgic, Yilmaz; Erdogan, Mehmet AliThe occurrence of spontaneous bacterial peritonitis (SBP) is significantly increased in carriers of nucleotide-binding oligomerization domain-containing protein 2 (NOD2) variants, suggesting that local immune alterations might be implicated in bacterial translocation (BT). We aimed to assess the role of the NOD2 gene in conferring susceptibility to SBP. We also sought to determine whether levels of serum interleukin-6 (IL-6), lipopolysaccharide-binding protein, and soluble TNF-alpha receptor, along with the presence of bacterial DNA (bactDNA) in ascitic fluid, are appropriate markers for BT in patients with liver cirrhosis and SBP. A cohort of 171 patients was divided into two groups: patients with SBP (n = 82) and those without SBP (n = 89). The presence of the most common NOD2 variants (p.R702W, p.G908R, and c.3020insC) was determined in these patients. We detected the p.G908R variant in four patients (4.9 %) of the SBP group. No significant difference was observed between the SBP and non-SBP groups for NOD2 risk variants. The frequency of bactDNA in ascitic fluid was higher for patients with NOD2 variants than for patients without variants (p = 0.021). Serum IL-6 levels in the SBP group were higher than those in the non-SBP group. The frequent detection of bactDNA in ascites of patients with the p.G908R variant suggests there is a strong association between NOD2 risk variants and BT in SBP patients. In addition, increased serum IL-6 levels and bactDNA in ascitic fluid could be considered surrogate markers for BT in patients with cirrhosis.