Protective mechanisms of anthocyanins from purple sweet potato against tert-butyl hydroperoxide-induced hepatotoxicity
Protective mechanisms of anthocyanins from purple sweet potato against tert-butyl hydroperoxide-induced hepatotoxicity
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DOI：
10.1016/j.fct.2011.05.021
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发表时间：
2011-09-01
影响因子：
4.3
通讯作者：
Jeong, Hye Gwang
中科院分区：
文献类型：
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作者：
Hwang, Yong Pil;Choi, Jae Ho;Jeong, Hye Gwang
花青素已被证明具有抗增殖、抗炎和抗癌作用。本文研究了紫甘薯花青素提取物（AF）对过氧化叔丁基（t-BHP）诱导的HepG2细胞株和大鼠肝脏毒性的保护作用。结果表明，通过丙二醛和谷胱甘肽的评价，在t-BHP治疗前口服房房炎预处理可显著降低血清肝酶标志物（ALT和AST）水平，降低肝脏氧化应激。肝脏的组织病理学评估也显示，房颤降低了肝脏病变的发生率。体外实验结果表明，通过细胞毒性、细胞内谷胱甘肽含量、脂质过氧化、活性氧（ROS）水平和半胱天冬酶活性测定，AF可显著降低t- bhp诱导的氧化损伤。同时，AF上调血红素加氧酶-1 （HO-1）、醌还原酶和谷胱甘肽s -转移酶等抗氧化酶。此外，AF诱导Nrf2核易位，Akt和ERK1/2激活，这些通路参与诱导Nrf2核易位。综上所述，这些结果表明，AF对t- bhp诱导的肝毒性的保护作用可能至少部分是由于其清除ROS和通过Akt和ERK1/2/Nrf2信号通路调节抗氧化酶HO-1的能力。(C) 2011 Elsevier Ltd.版权所有。
Anthocyanins have been shown to exert anti-proliferative, anti-inflammatory effects and anti-carcinogenic activity. In the present work, we investigated the protective effects of anthocyanin fraction (AF) from purple sweet potato on tert-butyl hydroperoxide (t-BHP)-induced hepatotoxicity in HepG2 cell line and in rat liver. The result showed that the oral pretreatment of AF before t-BHP treatment significantly lowered the serum levels of the hepatic enzyme markers (ALT and AST) and reduced oxidative stress of the liver by evaluation of malondialdehyde and glutathione. Histopathological evaluation of the livers also revealed that AF reduced the incidence of liver lesions. The in vitro result showed that AF significantly reduced t-BHP-induced oxidative injury, as determined by cell cytotoxicity, intracellular glutathione content, lipid peroxidation, reactive oxygen species (ROS) levels, and caspases activation. Also, AF up-regulated antioxidant enzymes including heme oxygenase-1 (HO-1), NAD(P)H:quinone reductase, and glutathione S-transferase. Moreover, AF induced Nrf2 nuclear translocation and Akt and ERK1/2 activation, pathways that are involved in inducing Nrf2 nuclear translocation. Taken together, these results suggest that the protective effects of AF against t-BHP-induced hepatotoxicity may, at least in part, be due to its ability to scavenge ROS and to regulate the antioxidant enzyme HO-1 via the Akt and ERK1/2/Nrf2 signaling pathways. (C) 2011 Elsevier Ltd. All rights reserved.