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Journal of Environmental Pathology, Toxicology and Oncology
インパクトファクター: 1.625 5年インパクトファクター: 1.63 SJR: 0.402 SNIP: 0.613 CiteScore™: 2.3

ISSN 印刷: 0731-8898
ISSN オンライン: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.2015013126
pages 175-182

Protective Effect of Infliximab Against Carbon Tetrachloride−Induced Hepatotoxicity

Ibrahim Sehitoglu
Department of Pathology, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey
Levent Tumkaya
Department of Histology and Embryology, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey
Recep Bedir
Department of Pathology, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey
Ender Ozer
Department of Surgery, Recep Tayyip Erdogan University, School of Medicine, Rize, Turkey
Medine Cumhur Cure
Department of Biochemistry, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey
Yildiray Kalkan
Department of Histology and Embryology, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey
Suleyman Yuce
Internal Medicine, Kumru State Hospital, Ordu, Turkey
Erkan Cure
Department of Internal Medicine, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey

要約

Carbon tetrachloride (CCl4), a solvent frequently used in industry, can cause acute liver failure and liver fibrosis. Infliximab (Ib), a potent tumor necrosis factor alpha blocker, has a protective effect on the liver. Therefore, we investigated the protective effect of Ib against CCl4-induced acute liver injury. In this study, 24 male Sprague Dawley rats were randomly divided into three groups: the control group (n = 8), the CCl4 group (n = 8), and the CCl4 + Ib group (n = 8). A single dose of 2 mL/kg CCL4 was administered to the CCL4 group. The CCl4 + Ib group was injected with a single dose (7 mg/kg) of Ib 24 h before CCl4 was administered. In the CCl4 group, the serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and the liver tissue levels of transforming growth factor beta 1 (TGF-β1), interleukin 1 beta (IL-1β), and adenosine deaminase (ADA) were significantly higher than the levels of these same substances in the control and CCl4 + Ib groups. The histopathological investigation revealed that although there was excessive liver injury in the CCl4 group, there was reduced injury in the CCl4 + Ib group. In addition, the carbamoyl phosphate synthetase I (CPS-I) and carbonic anhydrase II (CA-II) levels in the CCl4 group were significantly lower than those in the control and CCl4 + Ib groups. The results show that during CCl4-induced hepatotoxicity, Ib prevents liver injury by suppressing TGF-β1 and IL-1β levels, decreasing ADA levels, and regulating CPS-I and CA-II enzyme levels.


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