Basic & Translational - Original Article

Vol. 28 No. 5 (2017): 2017.28.5-Turkish Journal of Gastroenterology

Methylprednisolone prevents bacterial translocation in thioacetamide-induced liver failure in rats

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Murat Muhsin Muhip Harputluoğlu
İsmail Temel
Ulvi Demirel
Yüksel Seçkin
Murat Aladağ
Barış Otlu
Neşe Karadağ
Fatma Özyalın
Nilay Aydoğan
Engin Burak Selçuk

Abstract

Background/Aims: Steroids have been shown to prevent intestinal oxidative stress. We investigated the effects of methylprednisolone on intestinal oxidative damage and bacterial translocation in thioacetamide-induced liver failure in rats.<o:p></o:p>

Materials and Methods: Group 1 (n=8) was the control group. In group 2 (n=8), the thioacetamide group, rats received 300 mg/kg intraperitoneal thioacetamide daily for 2 days. In group 3 (n=8), the thioacetamide+methylprednisolone group, treatment with methylprednisolone (30 mg/kg intraperitoneal) was commenced 48 h before the first dose of thioacetamide. In group 4 (n=8), the methylprednisolone group, the rats received only methylprednisolone (30 mg/kg intraperitoneal).<o:p></o:p>

Results: Serious hepatic and intestinal oxidative damage and high bacterial translocation frequencies were observed in the thioacetamide group compared with those of the controls. Bacterial translocation frequency in the thioacetamide+methylprednisolone group was significantly lower than that in the thioacetamide group (p<0.05). Intestinal thiobarbituric acid-reactive substances and myeloperoxidase levels and tissue damage scores for the intestines in the thioacetamide+methylprednisolone group were lower than those in the thioacetamide group (p<0.01, p<0.01, and p<0.0001, respectively).

Conclusion: Our findings suggest that methylprednisolone reduces bacterial translocation by preventing intestinal oxidative damage in this model of acute liver failure in rats.
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Cite this article as: Harputluoğlu MMM, Temel İ, Demirel U, et al. Methylprednisolone prevents bacterial translocation in thioacetamide-induced liver failure in rats. Turk J Gastroenterol 2017; 28: 394-400.<o:p></o:p>

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