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        Preventive Effect of Probiotics and α-Tocopherol on Ethanol-Induced Gastric Mucosal Injury in Rats

        Altug Senol,Mehmet Isler,Aynur G. Karahan,Gulden B. Kilic,Hakan Kuleasan,Selcuk Kaya,Muharrem Keskin,Ibrahim Goren,Ulku Saritas,Buket C. Aridogan,Namik Delibas 한국식품영양과학회 2011 Journal of medicinal food Vol.14 No.1

        The protective effect of a probiotic mixture of 13 different bacteria and α-tocopherol on 98% ethanol-induced gastric mucosal injury was evaluated. Levels of gastric mucosal pro- and anti-inflammatory cytokines, malondialdehyde, and secretory immunglobulin A were measured. Rats were allocated into four groups: control, ethanol, probiotic, and α-tocopherol. The control and ethanol groups received skim milk for 14 days. Probiotic and α-tocopherol groups were administered probiotic mixture suspended in skim milk and 100mg/kg α-tocopherol, respectively, by daily gavage for 14 days. On Day 15, gastric lesions were induced by administration of ethanol 98% (1mL) to all rats except those in the control group. Probiotic, but not α-tocopherol, seemed to inhibit ethanol-induced gastric mucosal tumor necrosis factor-α, interferon-γ, and interleukin-2 production (P>.05). Ethanol caused the elevation of mucosal interleukin-4 level (compared to the control, P<.05). Probiotic pretreatment significantly suppressed the ethanol-induced increase of gastric mucosal interleukin-4 levels. Pretreatment with either probiotic or α-tocopherol inhibited the ethanol-induced increase of mucosal malondialdehyde concentration (P<.01 and P<.05, respectively). Probiotic pretreatment enhanced the gastric mucosal secretory immunoglobulin A concentration (P<.001). In conclusion, probiotic mixture and α-tocopherol reduced ethanol-induced gastric mucosal lipid peroxidation, suggesting that they may be beneficial for gastric lesions induced by lower ethanol concentration.

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        Investigation of pulmonary involvement in in­flammatory bowel disease in an experimental model of colitis

        ( Bunyamin Aydin ),( Yıldıran Songur ),( Necla Songur ),( Oguzhan Aksu ),( Altug Senol ),( I Metin Ciris ),( Recep Sutcu ) 대한내과학회 2016 The Korean Journal of Internal Medicine Vol.31 No.5

        Background/Aims: Inflammatory bowel disease (IBD) may also involve various extra-intestinal organs. Clinical studies have found asymptomatic/symptomatic pulmonary involvement in 1% to 6% of patients with IBD. The present study his­topathologically investigated pulmonary involvement in an experimental model of colitis in order to demonstrate pulmonary tissue involvement in IBD and to expose potential etiological factors. It also explored the relation between inflam­mation and tissue concentrations of vascular endothelial growth factor (VEGF) and tumor necrosis factor α (TNF-α). Methods: The study comprised 24 male Wistar albino rats. The rats were divided into four groups of six rats each. Acute colitis was induced in two separate groups using either the dextran sulphate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) method, while the other two groups were used as controls for each model of colitis. Wallace scoring was used for macroscopic assessment of colitis, and the lungs were histopathologically examined. Concentrations of VEGF and TNF-α in pulmonary tissue were measured by the enzyme-linked immunosorbent assay method. Results: The number of animals that had alveolar hemorrhage was significantly higher in the TNBS induced colitis and DSS-induced colitis groups compared to their own control groups (p = 0.015 and p = 0.015, respectively). VEGF and TNF-α concentrations in pulmonary tissues were significantly increased in both the TNBS colitis and DSS colitis groups compared to their own control groups (p = 0.002 and p = 0.004, respectively; and p = 0.002 and p = 0.002, respectively). Conclusions: The present study demonstrated that significant and serious histo­pathological changes directly associated with colitis occur in the lungs in IBD.

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