Long Miao, Yang Shu-Hua, Han Jian-Xin, Li Peng, Zhang Yi, Dong Shuang, Chen Xinliang, Guo Jiayi, Wang Jun, He Jian-Bin
Key Laboratory of Zoonosis of Liaoning Province, College of Animal Science & Veterinary Medicine, Shenyang Agricultural University, Shenyang 110866, China.
College of Animal Science and Technology, Jilin Agricultural University, Changchun 130118, China.
Int J Mol Sci. 2016 May 25;17(6):808. doi: 10.3390/ijms17060808.
Although grape-seed proanthocyanidin extract (GSPE) demonstrates strong anti-oxidant activity, little research has been done to clearly reveal the protective effects on the hepatotoxicity caused by zearalenone (ZEN). This study is to explore the protective effect of GSPE on ZEN-induced oxidative damage of liver in Kunming mice and the possible protective molecular mechanism of GSPE. The results indicated that GSPE could greatly reduce the ZEN-induced increase of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities. GSPE also significantly decreased the content of MDA but enhanced the activities of antioxidant enzymes SOD and GSH-Px. The analysis indicated that ZEN decreased both mRNA expression levels and protein expression levels of nuclear erythroid2-related factor2 (Nrf2). Nrf2 is considered to be an essential antioxidative transcription factor, as downstream GSH-Px, γ-glutamyl cysteine synthetase (γ-GCS), hemeoxygenase-1 (HO-1), and quinone oxidoreductase 1 (NQO1) decreased simultaneously, whereas the pre-administration of GSPE groups was shown to elevate these expressions. The results indicated that GSPE exerted a protective effect on ZEN-induced hepatic injury and the mechanism might be related to the activation of the Nrf2/ARE signaling pathway.
尽管葡萄籽原花青素提取物（GSPE）具有很强的抗氧化活性，但关于其对玉米赤霉烯酮（ZEN）所致肝毒性的保护作用的研究却很少。本研究旨在探讨GSPE对ZEN诱导的昆明小鼠肝脏氧化损伤的保护作用及其可能的保护分子机制。结果表明，GSPE能显著降低ZEN诱导的血清天冬氨酸转氨酶（AST）和丙氨酸转氨酶（ALT）活性升高。GSPE还能显著降低丙二醛（MDA）含量，但提高抗氧化酶超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）的活性。分析表明，ZEN降低了核红细胞2相关因子2（Nrf2）的mRNA表达水平和蛋白表达水平。Nrf2被认为是一种重要的抗氧化转录因子，其下游的谷胱甘肽过氧化物酶（GSH-Px）、γ-谷氨酰半胱氨酸合成酶（γ-GCS）、血红素加氧酶-1（HO-1）和醌氧化还原酶1（NQO1）同时降低，而预先给予GSPE组则显示这些表达升高。结果表明，GSPE对ZEN诱导的肝损伤具有保护作用，其机制可能与激活Nrf2/ARE信号通路有关。
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