Anthocyanins from purple sweet potato attenuate dimethylnitrosamine-induced liver injury in rats by inducing Nrf2-mediated antioxidant enzymes and reducing COX-2 and iNOS expression

作者:Hwang Yong Pil; Choi Jae Ho; Yun Hyo Jeong; Han Eun Hee; Kim Hyung Gyun; Kim Jin Young; Park Bong Hwan; Kh**** Tilak; Choi Jun Min; Chung Young Chul; Jeong Hye Gwang*
来源:Food and Chemical Toxicology, 2011, 49(1): 93-99.
DOI:10.1016/j.fct.2010.10.002

摘要

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.

  • 出版日期2011-1