Department of Toxicology, College of Pharmacy, Chungnam National University, Daejeon, Republic of Korea.
Food Chem Toxicol. 2011 Jan;49(1):93-9. doi: 10.1016/j.fct.2010.10.002. Epub 2010 Oct 8.
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 GSTα, 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-κB) 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-κB inhibition.
紫薯中的花色苷通过多种生化机制表现出抗氧化和保肝活性。然而，花色苷诱导抗氧化酶对抗慢性肝损伤作用的信号通路尚不完全清楚。我们研究了紫薯花色苷（AF）是否可以通过核红细胞 2 相关因子 2（Nrf2）途径诱导抗氧化剂和减少炎症来预防二甲基亚硝胺（DMN）诱导的肝损伤。AF 处理可减轻 DMN 诱导的血清丙氨酸氨基转移酶和天冬氨酸氨基转移酶活性升高。它还可防止肝丙二醛的形成和谷胱甘肽的耗竭，并维持 DMN 中毒大鼠肝脏中正常的谷胱甘肽-S-转移酶（GST）活性。此外，AF 增加了 Nrf2、NADPH：醌氧化还原酶-1、血红素加氧酶-1 和 GSTα 的表达，这些表达在 DMN 作用下降低，并降低了环氧合酶-2 和诱导型一氧化氮合酶的表达。在 DMN 诱导的肝损伤组中观察到核因子 kappa B（NF-κB）的核易位增加，但 AF 抑制了这种易位。总之，这些结果表明，AF 通过 Nrf2 途径增加抗氧化酶和 Nrf2 的表达，同时通过 NF-κB 抑制减少炎症介质的表达。这些数据表明，AF 通过 Nrf2 途径诱导抗氧化防御，并通过抑制 NF-κB 减少炎症。
