4.7 Article

Protective mechanisms of anthocyanins from purple sweet potato against tert-butyl hydroperoxide-induced hepatotoxicity

期刊

FOOD AND CHEMICAL TOXICOLOGY
卷 49, 期 9, 页码 2081-2089

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2011.05.021

关键词

Purple sweet potato; Anthocyanins; tert-butyl hydroperoxide; Nrf2; Hepatoprotection

资金

  1. Technology Development Program for Agriculture and Forestry [108159-3]
  2. Ministry for Food, Agriculture, Forestry and Fisheries
  3. National Research Foundation of Korea (NRF)
  4. Ministry of Education, Science and Technology, Republic of Korea [2009-0093815]

向作者/读者索取更多资源

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.

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