Sehitoglu Ibrahim, Tumkaya Levent, Bedir Recep, Ozer Ender, Cure Medine Cumhur, Kalkan Yildiray, Yuce Suleyman, Cure Erkan
Department of Pathology, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey.
Department of Histology and Embryology, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey.
J Environ Pathol Toxicol Oncol. 2015;34(2):175-82. doi: 10.1615/jenvironpatholtoxicoloncol.2015013126.
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.
四氯化碳（CCl4）是一种工业上常用的溶剂，可导致急性肝衰竭和肝纤维化。英夫利昔单抗（Ib）是一种强效的肿瘤坏死因子α阻滞剂，对肝脏具有保护作用。因此，我们研究了Ib对CCl4诱导的急性肝损伤的保护作用。在本研究中，24只雄性Sprague Dawley大鼠被随机分为三组：对照组（n = 8）、CCl4组（n = 8）和CCl4 + Ib组（n = 8）。CCl4组给予单剂量2 mL/kg的CCL4。CCl4 + Ib组在给予CCl4前24小时注射单剂量（7 mg/kg）的Ib。在CCl4组中，天冬氨酸转氨酶（AST）和丙氨酸转氨酶（ALT）的血清水平，以及转化生长因子β1（TGF-β1）、白细胞介素1β（IL-1β）和腺苷脱氨酶（ADA）的肝组织水平显著高于对照组和CCl4 + Ib组中这些相同物质的水平。组织病理学研究显示，虽然CCl4组存在过度的肝损伤，但CCl4 + Ib组的损伤有所减轻。此外，CCl4组中的氨甲酰磷酸合成酶I（CPS-I）和碳酸酐酶II（CA-II）水平显著低于对照组和CCl4 + Ib组。结果表明，在CCl4诱导的肝毒性过程中，Ib通过抑制TGF-β1和IL-1β水平、降低ADA水平以及调节CPS-I和CA-II酶水平来预防肝损伤。
