Protective Effect of Infliximab Against Carbon Tetrachloride-Induced Hepatotoxicity


Sehitoglu I., TUMKAYA L., Bedir R., Ozer E., Cure M. C., Kalkan Y., ...More

JOURNAL OF ENVIRONMENTAL PATHOLOGY TOXICOLOGY AND ONCOLOGY, vol.34, no.2, pp.175-182, 2015 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 34 Issue: 2
  • Publication Date: 2015
  • Doi Number: 10.1615/jenvironpatholtoxicoloncol.2015013126
  • Journal Name: JOURNAL OF ENVIRONMENTAL PATHOLOGY TOXICOLOGY AND ONCOLOGY
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.175-182
  • Keywords: carbon tetrachloride, acute liver failure, carbamoyl phosphate synthetase I, carbonic anhydrase II, interleukin 1 beta, transforming growth factor beta 1, ADENOSINE-DEAMINASE, XANTHINE-OXIDASE, OXIDATIVE DAMAGE, NITRIC-OXIDE, LIVER-INJURY, RATS, MALONDIALDEHYDE, TOPIRAMATE, CIRRHOSIS, TOXICITY
  • Recep Tayyip Erdoğan University Affiliated: Yes

Abstract

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-beta 1), interleukin 1 beta (IL-1 beta), 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-beta 1 and IL-1 beta levels, decreasing ADA levels, and regulating CPS-I and CA-II enzyme levels.