Hepatoprotective effects of allyl isothiocyanate against carbon tetrachloride-induced hepatotoxicity in rat
Hepatoprotective effects of allyl isothiocyanate against carbon tetrachloride-induced hepatotoxicity in rat
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DOI：
10.1016/j.cbi.2016.05.037
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发表时间：
2016-07-25
影响因子：
5.1
通讯作者：
Shin, Taekyun
中科院分区：
文献类型：
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作者：
Ahn, Meejung;Kim, Jeongtae;Shin, Taekyun
我们评价了异硫氰酸烯丙酯（AITC）对四氯化碳（CCl4）诱导的大鼠肝损伤的保护作用。大鼠分别以5 （AITC 5）和50 (AITC 50) mg/kg体重口服AITC，每日1次，连续3天，同时或不同时腹腔注射CCl4。血清化学检测谷丙转氨酶（ALT）和天冬氨酸转氨酶（AST）的变化。采用实时聚合酶链反应检测肝组织超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、丙二醛（MDA）活性，分析促炎因子肿瘤坏死因子- α (tnf - α)、白细胞介素-1 β (IL-1 β) mRNA表达。Western blot和免疫组织化学分别评价血红素加氧酶-1 （HO-1）和离子钙结合蛋白-1 （Iba-1）的免疫反应性。血清化学方面，口服AITC本身不影响血清ALT和AST水平，而AITC 5和AITC 50预处理可显著降低ccl4中毒大鼠升高的ALT和AST活性水平。此外，与CCl4组相比，AITC显著抑制了SOD和CAT的降低，MDA、tnf - α mRNA的表达升高，诱导了HO-1的表达。组织病理学评估和Iba-1免疫反应性也支持AITC对ccl4诱导的肝损伤的肝保护作用。这些结果表明，AITC可能通过减少脂质过氧化、增强抗氧化酶和抑制库普弗细胞和巨噬细胞来改善氧化性肝损伤。2016爱思唯尔爱尔兰有限公司版权所有。
We evaluated the hepatoprotective activity of allyl isothiocyanate (AITC) against carbon tetrachloride (CCl4)-induced liver injury in rats. Sprague Dawley rats were orally administered AITC at doses of 5 (AITC 5) and 50 (AITC 50) mg/kg body weight once daily for 3 days, with or without intraperitoneal injection of CCl4. Serum chemistry was assessed for changes in alanine aminotransferase (ALT) and aspartate aminotransferase (AST). The enzyme activities of superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) were examined in liver tissues, while pro-inflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) mRNA expression were analyzed using real-time polymerase chain reaction. And heme oxygenase-1 (HO-1) and ionized calcium binding protein-1 (Iba-1) immunoreactivities were evaluated by Western blot analysis and immunohistochemistry, respectively. In serum chemistry, the oral administration of AITC itself did not affect the serum levels of ALT or AST, furthermore pretreatment with AITC 5 and AITC 50 significantly reduced the ALT and AST activity levels that were elevated in CCl4-intoxicated rats. In addition, AITC significantly suppressed the reduction of SOD and CAT, and the elevation of MDA, TNF-alpha mRNA expression, on the other hands, induced the expression of HO-1 compared with those of the vehicle-treated CCl4 group. The histopathological evaluation and Iba-1 immunoreactivity also supported the hepatoprotective effects of AITC against CCl4-induced liver injury. These results suggest that AITC ameliorates oxidative liver injury, possibly through reducing lipid peroxidation, enhancing antioxidant enzymes, and suppressing Kupffer cells and macrophages. (C) 2016 Elsevier Ireland Ltd. All rights reserved.