Journal
FOOD AND CHEMICAL TOXICOLOGY
Volume 49, Issue 1, Pages 93-99Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2010.10.002
Keywords
Purple sweet potato; Anthocyanins; DMN; Inflammation; Antioxidant enzymes; Nrf2
Categories
Funding
- Ministry for Food, Agriculture, Forestry and Fisheries [108159-3]
- National Research Foundation of Korea (NRF) funded by Ministry of Education, Science and Technology, Republic of Korea [2009-0093815]
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Anthocyanins of the purple sweet potato exhibit antioxidant and hepatoprotective activities via a multitude of biochemical mechanisms. However, the signaling pathways involved in the actions of anthocyanin-induced antioxidant enzymes against chronic liver injury are not fully understood. We examined whether an anthocyanin fraction (AF) from purple sweet potato may prevent dimethylnitrosamine (DMN)-induced liver injury by inducing antioxidants via nuclear erythroid 2-related factor 2 (Nrf2) pathways and by reducing inflammation. Treatment with AF attenuated the DMN-induced increased serum alanine aminotransferase and aspartate aminotransferase activities. It also prevented the formation of hepatic malondialdehyde and the depletion of glutathione and maintained normal glutathione-S-transferase (GST) activity in the livers of DMN-intoxicated rats. Furthermore, AF increased the expression of Nrf2, NADPH:quinine oxidoreductase-1, heme oxygenase-1, and GST alpha, which were reduced by DMN, and decreased the expression of cyclooxygenase-2 and inducible nitric oxide synthase. An increase in the nuclear translocation of nuclear factor kappa B (NF-kappa B) was observed in the DMN-induced liver injury group, but AF inhibited this translocation. Taken together, these results demonstrate that AF increases the expression of antioxidant enzymes and Nrf2 and at the same time decreases the expression of inflammatory mediators in DMN-induced liver injury. These data imply that AF induces antioxidant defense via the Nrf2 pathway and reduces inflammation via NF-kappa B inhibition. (c) 2010 Elsevier Ltd. All rights reserved.
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